Management of Bell’s Palsy and

Ramsay Hunt Syndrome

Of the multitude of causes of facial paralysis, Bell’s palsy and Ramsay
Hunt syndrome are two of the most common. Bell’s palsy alone
accounts for almost three-quarters of all acute facial palsies. Although
the diagnosis of Ramsay Hunt syndrome is generally obvious, a
thorough evaluation and close follow-up are required to establish a firm
diagnosis of Bell’s palsy. This chapter discusses the pathology,
pathophysiology, epidemiology, evaluation, and management of these
common disorders.

Bell’S Palsy
Bell (1774–1842) first described a patient with facial paralysis in 1818;
subsequently, all patients with facial palsy of unknown etiology have
come to bear his name. The etiology of this “idiopathic” disorder has
become much clearer in recent years. Although first proposed in 1972
by McCormick, herpes simplex virus (HSV) has only recently been
identified as the disease vector, and an animal model has been
designed. Murakami et al. identified HSV type 1 (HSV-1) DNA
fragments in the perineural fluid in 11 of 14 patients undergoing facial
nerve decompression. In this study, no control subjects had HSV-1 DNA
in the perineural fluid. Using polymerase chain reaction to analyze the
saliva of patients with Bell’s palsy, Furuta et al. identified HSV-1 DNA in
50% of patients, which was significantly more often than controls, a
finding confirmed by other groups. Polymerase chain reaction has also
been used to isolate HSV-1 genomic DNA from the geniculate ganglion
of a temporal bone in a patient dying during the acute phase of Bell’s
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 palsy.

Sugita et al. proposed an animal model of BP. Six days after the
inoculation of HSV-1 into the auricle or tongue of mice, a temporary
ipsilateral facial paralysis was identified that recovered spontaneously
within 3 to 7 days. Histopathologically, neural edema, vacuolar
degeneration, and inflammatory cell infiltration with associated
demyelination or axonal degeneration were observed in the affected
facial nerve and nucleus. HSV-1 antigens were identified within the
facial nerve, geniculate ganglion, and facial nucleus 6 to 20 days after
inoculation. Similar pathological findings have been shown in rabbits
after HSV-1 inoculation, but without the associated facial paralysis.

The histopathological changes observed in autopsy specimens of

patients who died with acute idiopathic facial paralysis have provided
some insight into the underlying cellular mechanisms in Bell’s palsy.
Reddy et al. found degeneration of the myelin sheath and axons,
perivascular inflammation, and a phagocytic cell infiltrate in 10% to
30% of nerve fibers in a patient 17 days after the onset of an acute
idiopathic facial paralysis. Fowler found diffuse vascular engorgement
throughout the intratemporal facial nerve and evidence of acute
hemorrhage within the intracanalicular, labyrinthine, and geniculate
portions of the facial nerve in a patient who died shortly after the onset
of Bell’s palsy. In examining an autopsy specimen of a patient who died
13 days after the onset of Bell’s palsy, McKeever et al. found diffuse
lymphocytic infiltration of the intratemporal facial nerve with ongoing
myelin phagocytosis. They later reexamined the same specimen and
noted that the most pronounced lymphocytic infiltration of the nerve
was at the labyrinthine segment, findings that they believed were most
consistent with an ongoing compression-type injury to the facial nerve.
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 Multiple reports have found that there seems to be evidence of
constriction of the nerve at the meatal foramen (MF) in cases of Bell’s
palsy. In specimens examined during the acute phase of Bell’s palsy,
lymphocytic infiltration, perineural edema, and myelin degeneration
have been noted. , In a nerve specimen examined 1 year after the
diagnosis of Bell’s palsy lymphocytic infiltration, perineural edema and
fibrotic changes were noted. Intraoperative biopsy specimens of the
greater superficial petrosal nerve from patients undergoing nerve
decompression procedures for Bell’s palsy have shown axonal
demyelination and degeneration with lymphocytic infiltration. Together,
the histopathological findings in Bell’s palsy show demyelination and
axonal loss with lymphocytic or phagocytic infiltration, findings that
appear more pronounced at the labyrinthine segment of the facial
nerve.

Considering this evidence, the pathogenesis of Bell’s palsy becomes

more apparent: a virally induced inflammatory response that produces
edema within the nerve. Fisch and Felix first proposed that the facial
nerve was entrapped at the MF as a result of neural edema.
Intraoperative conduction studies have shown an electrophysiological
blockage at this site. The constriction imposed produces a conduction
block at first; however, with prolonged or increased constriction,
ischemia results. Subsequently, Wallerian degeneration occurs,
producing axonotmesis, neurotmesis, or both. A spectrum of injury
within the nerve from neurapraxia to neurotmesis may occur in Bell’s
palsy. , The proportion of each of these determines the amount of facial
function that returns when the acute phase of the disease subsides.

Bell’s palsy accounts for nearly three-quarters of all acute facial palsies.
The incidence of Bell’s palsy is 20 to 30 cases per 100,000 per year.
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 The median age is 40 years, but it can occur at any age. The incidence
is highest in patients older than 70 years and lowest in children younger
than 10 years. The left and right sides are equally affected. Men and
women are equally affected, but there is a higher incidence of Bell’s
palsy in pregnant women (45 cases per 100,000).

The clinical presentation of Bell’s palsy is well known; however, the

clinician must exclude other causes of facial paralysis based on the
history and physical examination findings. Patients describe an acute
onset of unilateral paresis that occurs within less than 72 hours. The
paresis can progress to complete paralysis over 1 to 7 days. Bilateral
involvement, either simultaneously or consecutively, has been
described. A history of progression of weakness over weeks to months,
recurrent episodes of paralysis, and twitching of the facial muscles
should not be considered symptoms of Bell’s palsy. Other associated
symptoms of hearing loss, vestibular symptoms, or other cranial nerve
neuropathies also exclude the diagnosis of Bell’s palsy.

On physical examination, the patient displays unilateral weakness or

flaccid paralysis of all branches of the facial nerve. If the forehead
movement is normal and there is strong eye closure and symmetric
blinking, a central origin of paralysis should be suspected. The
tympanic membrane should have normal color and mobility. Careful
bimanual palpation of the parotid gland may reveal a deep lobe parotid
neoplasm. Oral cavity examination may show a loss of papillae on the
ipsilateral tongue. Cranial nerve (CN) testing is normal with the
exception of the involved CN VII. Serial examinations are essential; if
some evidence of recovery is not noted within 3 to 6 months, an
aggressive search for an underlying neoplasm should be undertaken.

Audiometric evaluation should reveal symmetric function except for an

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 absent ipsilateral acoustic reflex. If unilateral hearing loss or acoustic
reflex decay is present, further evaluation for retrocochlear pathology is
necessary. If vestibular complaints are present, an
electronystagmogram is performed, and a diagnosis of Bell’s palsy
should be questioned. If the history and clinical presentation are highly
suggestive of Bell’s palsy, magnetic resonance imaging (MRI) and
computed tomography (CT) are not performed. High-resolution CT
scans and MRIs are obtained if patients have associated symptoms of
otorrhea, vestibular complaints, and hearing loss. Planned surgical
decompression and persistent dense paralysis after 6 months are also
indications for imaging. Serologic tests for Lyme disease
(immunoglobulin G or M) are an important part of the work-up for
unexplained facial paralysis in endemic areas. Serologic testing for
antibodies to HSV or varicella zoster has provided some correlative
evidence for a viral etiology in Bell’s palsy, although laboratory
investigations in general have not been found to provide clinically
relevant data and routine serological testing is not currently
recommended.

Electrodiagnostic testing is an important element of the diagnostic

evaluation of facial paralysis. Testing can determine the extent of facial
nerve injury and provide useful prognostic information for the
development of management strategies. The technique of
electroneuronography (ENoG), developed by Esslen, can estimate the
proportion of nerve fibers that have undergone Wallerian degeneration
from those fibers that are temporarily blocked (neurapraxia). ENoG
testing is not performed until 3 to 4 days after the development of
complete unilateral paralysis because Wallerian degeneration does not
become apparent until 48 to 72 hours after an acute injury to the nerve.
Electrodiagnostic testing is not performed when the patient exhibits
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 paresis only. The presence of voluntary movement 4 to 5 days after the
onset of paresis indicates only minor injury, and complete recovery
should be anticipated.

ENoG is most accurate when it is performed within 3 weeks of the

acute injury. The test is performed using standard electromyography
(EMG) equipment but requires the use of special surface stimulating
and recording electrodes. The recording electrodes are placed in a
hand-held carrier and manipulated in the nasolabial fold with the Esslen
technique. The recording electrodes are not taped to the skin, as has
been described by others.

An evoked electric stimulus generates synchronous facial muscle

movement that can be recorded from the skin surface [termed the
compound muscle action potential (CMAP)]. The amplitude of the
biphasic CMAP has been found to correlate with the number of blocked
or neurapraxic nerve fibers. As the percentage of degenerated fibers
within the nerve increases, the amplitude of the CMAP decreases
compared with the normal side of the face. Fisch and Esslen
determined that if 90% or more of the fibers within the facial nerve
degenerate within the first 14 days of an acute paralysis, a severe injury
has occurred and the chances of complete recovery are less than 50%.
Patients who do not reach the 90% degeneration level by 3 weeks have
a very good prognosis and are likely to regain normal facial motion
without synkinesis. The time course of degeneration is also important;
the more rapid the degeneration, the more severe the injury. A patient
showing greater than 90% degeneration at 5 days would have a worse
prognosis than a patient with 90% degeneration at 14 days.

Patients exhibiting 90% to 100% degeneration or no response to

electric stimulation, in addition to ENoG, must undergo EMG testing. An
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 EMG needle is placed in the orbicularis oris and oculi muscles, and the
patient is asked to make a forceful contraction. Any voluntary motor
unit activity indicates deblocking of the conduction block and portends
a favorable prognosis. When deblocking occurs, fibers may not
discharge at the same rate because of the previous injury, and may fail
to generate a surface CMAP, resulting in a false-positive test result on
ENoG testing. As movement returns to the face, the surface CMAP may
also be absent for the same reason. Voluntary evoked EMG testing is
mandatory if a surgical decompression is planned. If a facial paralysis
has been slowly progressive over weeks to months, degeneration and
regeneration of nerve fibers occur within the nerve, resulting in similar
dyssynchronous discharge of evoked impulses and an inaccurate
CMAP recording.

Topognostic testing is widely reported to be useful in determining the

site of injury in acute facial paralysis; however, intraoperative studies
have shown that the Schirmer test is not accurate in diagnosing Bell’s
palsy. The Schirmer test may be used to determine the extent of
lacrimation and the need for eye protection.

A review of the natural history of Bell’s palsy shows that approximately

85% of patients begin to display some return of facial movement within
3 weeks of the onset of paresis. The remaining 15% begin to improve 3
to 6 months after the onset of the disease. Most patients show a
complete return of facial function, but 10% to 15% have residual
unilateral weakness and develop the secondary deformities of
synkinesis, epiphora, or contracture. Some motion returns in almost all
individuals with Bell’s palsy by 6 months. If no movement returns, a
vigorous search for another etiology should begin.

The management of patients with Bell’s palsy varies depending on the

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 type of specialist initially seeing the patient and on the training of the
individual specialist. Fig. 26.1 presents an overview of our management
strategy. Patients presenting within the first week of facial weakness
with paresis are placed on steroid therapy (prednisone, 60 to 80
mg/day for 7 days) and an antiviral agent (valacyclovir, 500 mg three
times per day for 10 days). If patients are seen 7 to 10 days after onset
and motor function is stable or improving, medical treatment is
unnecessary. Patients are instructed to return in 1 week for reevaluation
to determine if neural degeneration has occurred. Electrodiagnostic
testing is unnecessary as long as voluntary facial movement is present.
If total paralysis occurs in the interim, the total paralysis protocol of Fig.
26.1 is followed. Stable or improving patients are seen in 1 month.

Fig. 26.1

Algorithm for the management of Bell’s palsy. ENoG , Electroneuronography; MCF , middle
cranial fossa.

The use of steroids in Bell’s palsy has been the subject of much debate.
Numerous studies of varying designs in adults have shown better
outcomes in patients treated with steroids, , , especially when initiated
early in the course of the disease. Other randomized studies and meta-
analyses, including many studies in children, have concluded that
steroids did not affect the ultimate facial function outcomes in Bell’s
palsy. Grogan and Gronseth, in a comprehensive, evidence-based
review, concluded that there appeared to be a beneficial effect from
the use of steroids in Bell’s palsy. Ramsey et al. performed a meta-
analysis of 47 trials of steroid therapy for Bell’s palsy and concluded
that there seemed to be improved odds of recovery in patients treated
with steroids (49% to 97%) compared with untreated controls (23% to
64%). We use prednisone in a dose of 1 mg/kg daily for 7 days in all
cases in which it is not medically contraindicated, in anticipation of
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 speeding recovery, reducing the number of degenerating axons, and
reducing the number of patients needing decompression.

The combination of steroids and antivirals may be superior to either

one alone, although this remains a source of controversy in the
literature. A double-blind, randomized, controlled trial of acyclovir and
prednisone versus prednisone alone in the treatment of Bell’s palsy
showed better results with the combination therapy. This study
documented poor facial function recovery in 23% of patients in the
prednisone-only group compared with 7% in the acyclovir-plus-
prednisone group. Interpreting the results of this study, Grogan and
Gronseth reported that patients who receive antiviral therapy in
addition to steroids were 1.22 times as likely to have a good facial nerve
outcome. A multicenter, randomized, placebo-controlled study by Hato
et al. comparing treatment of patients with Bell’s palsy with steroids
and antivirals with treatment with steroids alone concluded that the
addition of valacyclovir improved the recovery rate from 75% to 90% in
cases of complete palsy, and from 89% to 96% in all cases of facial
palsy. Many other reviews of the topic have made similar conclusions.
Conversely, two multicenter, double-blind, placebo-controlled trials
found no significant improvement in facial nerve outcomes with the
addition of antiviral medications alone or in combination with
corticosteroids. ,

When these studies , , , are taken as a whole, the question of whether

antiviral medications benefit patients with Bell’s palsy remains a source
of contention. Careful analysis of the results from Hato et al. reveals
that the benefit of valacyclovir appears to vary with the severity of
facial nerve dysfunction with an absolute risk reduction (ARR) of 15.1%
for those with complete facial paralysis, 5.7% of those with severe
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 facial palsy, and no ARR for those with moderate facial dysfunction.
One explanation for why studies by Sullivan and Engström failed to
demonstrate benefit from treatment with antiviral medications could be
that in an effort to recruit large numbers of subjects, many patients with
mild to moderate facial paresis were included. Patients with mild facial
paresis are known to have a high rate of complete recovery and this
may have mitigated the effect of the antiviral medications. When
comparing the extent of facial palsy, patients enrolled by Hato et al. had
more severe facial dysfunction (House-Brackmann grades IV to V) than
did those enrolled by Sullivan (House-Brackmann grade 3.6).
Integrating the overall results from the aforementioned studies and
careful subgroup examination, it seems possible that antiviral
medications may offer therapeutic benefit to those with severe facial
nerve dysfunction and is of little aid to those with mild to moderate
facial paresis.

Other studies have found no significant difference between this

combination of drugs and the natural history of the disease. , One study
found a negative impact of treatment of patients with Bell’s palsy with
antivirals alone versus steroids alone. Because of the paucity of
potential side effects and good patient tolerance of antiviral
medications, the addition of antiviral medications to steroids in the
treatment of patients with Bell’s palsy seems prudent, especially in
those presenting with complete facial paralysis.

Patients presenting within 1 week of the onset of total unilateral

paralysis undergo electrodiagnostic testing (if at least 3 days have
passed since the onset of paralysis) and are started on medical
therapy. If the patient is seen in the first 3 days after the onset of
paralysis, steroid and antiviral therapy are initiated, and follow-up
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 electrodiagnostic studies are arranged. The frequency of follow-up
electrodiagnostic examinations is determined by the result of testing
and the time interval after paralysis, as suggested by Fisch ( Fig. 26.2 ).
Patients exhibiting nearly 90% neural degeneration on ENoG
examination, or who are degenerating quickly, undergo frequent
electrodiagnostic testing (every 1 or 2 days). If degeneration of greater
than 90% is reached, and there are no motor unit potentials on
voluntary EMG testing, the patient is considered a candidate for middle
cranial fossa decompression. When 90% degeneration is not reached
within 2 weeks (14 days) after the onset of paralysis, no further
electrodiagnostic studies need to be performed. Patients seen for the
first time more than 2 weeks after the onset of paralysis undergo EMG
evaluation to determine if regeneration has begun. They are scheduled
for a 6-month follow-up to ensure that some motor function has
returned. If no movement is evident at 6 months, it must be assumed
that Bell’s palsy was an incorrect diagnosis, and a search for another
disease process is initiated. The other etiologies of facial nerve
paralysis include traumatic, congenital, stroke, neoplasm, metastatic
lesion to the facial nerve, metabolic disease, infectious disease (e.g.,
Lyme disease, zoster), autoimmune (e.g., Guillain–Barré syndrome) and
systemic disease (e.g., sarcoidosis). Rare cases of idiopathic recurrent
facial nerve paralysis have been reported; the entity affects 4-7% of
patients who develop acute, nontraumatic facial nerve paralysis.
Clinical presentation shows much heterogeneity, with variable age at
presentation, number of facial paralysis episodes, and time interval
between facial nerve paralysis episodes. Electrodiagnostic testing is
not routinely performed, as patients often present between episodes of
recurrent facial nerve paralysis. Sullivan et al. demonstrated that
decompression of the facial nerve may be a reliable therapeutic
modality to decrease the number of facial nerve paralysis episodes and
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 also to improve facial nerve functional status. In the study ( n =11), the
average number of facial palsy episodes was 3.5 preoperatively
compared with 0 postoperatively at an average follow-up of 6.5 years.
The timing of decompression of this population is different to that of
Bell’s palsy in that they usually present after the 3-week window that is
followed in Bell’s palsy. The decompression can occur at the time of
another episode without ECoG findings or even in a period of
quiescence. Unfortunately, with this disorder, recovery worsens
following multiple episodes of paralysis.

Fig. 26.2

Recommended electroneuronography (ENoG) testing schedule in acute facial paralysis.

Ramsay Hunt Syndrome

Herpes zoster oticus refers to a syndrome of acute otalgia
accompanied by a herpetic vesicular rash. When accompanied by facial
paralysis, the syndrome is known as Ramsay Hunt syndrome. Ramsay
Hunt syndrome is the second most common cause of facial paralysis
(after Bell’s palsy), and is induced by the reactivation of the varicella
zoster virus that remains latent in the geniculate ganglion after primary
infection with chickenpox. Classically, patients present with severe
otalgia and unilateral facial paralysis. Vesicular eruptions may or may
not be present initially, but usually appear within 3 to 5 days of the
paralysis. The vesicular lesions can appear on the concha, ear canal,
postauricular skin, and tympanic membrane. Occasionally, the oral
cavity, neck, and shoulder are also involved. The disease can affect
other cranial nerves, including the auditory, vestibular, trigeminal,
glossopharyngeal, and vagus nerves, prompting the name herpes
zoster cephalicus .
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 Additionally, in contrast to Bell’s palsy, the symptoms are more severe
and the prognosis worse in Ramsay Hunt syndrome. The frequency of
complete neural degeneration of the facial nerve is substantially higher
than that in Bell’s palsy, and complete recovery of the facial motor
function has ranged from 10% to 31% in several studies. Patients with
auditory and vestibular dysfunction in addition to facial paralysis
generally have a worse prognosis. In addition, patients with diabetes,
hypertension, and advanced age have been reported to have a poorer
prognosis in Ramsay Hunt syndrome.

The diagnosis of Ramsay Hunt syndrome is based on the history of

otalgia, vesicular lesions or eschars, and facial paralysis. MRI typically
shows the enhancement of a large portion of the facial nerve, often the
vestibular and cochlear nerves, the labyrinth, and the dura lining the
internal auditory canal (IAC). Imaging as part of routine evaluation is
unnecessary. Electrodiagnostic studies have been unreliable in herpes
zoster oticus .

The management of Ramsay Hunt syndrome has changed with the

development of antiviral agents. The natural history of the disease was
evaluated by Devriese and Moesker, who identified only a 10% rate of
complete facial nerve recovery. Many studies have identified a superior
recovery rate of 75% using a combination of steroids and antiviral
agents. , The benefit of early initiation of steroid and antiviral treatment
was clearly shown in a study by Murakami et al., in which 75% of
patients treated within 3 days of the onset had complete recovery,
whereas only 30% of patients treated after 7 days experienced
complete recovery. We have experienced similar successful results
using intravenous acyclovir (10 mg/kg 3 times daily), oral acyclovir (800
mg, 5 times daily), or oral valacyclovir (500 mg 3 times daily) for 10
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 days, in combination with a 3-week tapering course of prednisone (60
to 80 mg/kg daily). Patients report a rapid reduction in pain and
occasionally experience the return of facial movement during the
medical therapy. Because of the presence of “skip” regions and diffuse
neuritis of the facial nerve, , surgical decompression of Ramsey Hunt
syndrome is not recommended.

Facial Nerve Decompression For Bell’S Palsy

Decompression of the facial nerve in Bell’s palsy has been reported
since the 1930s and is recommended in patients who exhibit greater
than 90% degeneration on ENoG and no voluntary EMG activity within
14 days of the paralysis. Preliminary results suggested that early
decompression of the labyrinthine, geniculate, and tympanic segments
of the facial nerve through a middle cranial fossa approach improves
recovery in severely degenerated cases, whereas decompression of
the mastoid segment alone did not alter the natural history of the
disease. Gantz et al. showed a statistically significant difference in
facial nerve outcome when decompression is performed within 2 weeks
of onset of the paralysis. The patients undergoing decompression
exhibited House-Brackmann grade I ( n = 14) or II ( n = 17) in 91% of
cases; two patients had a grade III, and one patient had a grade IV
outcome. No grade V or VI results were observed in the surgical group.
The patients who met surgical criteria but elected not to undergo
surgery had a 58% chance of a poor outcome. Within the nonsurgical
group, 19 patients had a House-Brackmann grade of either III or IV at
the 7-month follow-up. Recently, Cannon et al. confirmed that facial
nerve decompression is safe and efficacious. Five of 14 patients had
House-Brackmann grade I, five had grade II, and the remaining four had
grade III. Although this study did not directly compare surgical and
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 nonsurgical patients, it demonstrates that patients undergoing facial
nerve decompression typically have good outcomes with low morbidity.
This report reinforces the concept that individuals with severe
degeneration of the facial nerve, documented with the objective ENoG,
have better outcomes with decompression of the labyrinthine segment
and MF of the fallopian canal.

Intraoperative evoked EMG is used to localize the region of the

conduction block. Intraoperative direct nerve stimulation is useful when
the nerve is not completely degenerated, which includes most
instances when preoperative ENoG reveals 100% degeneration. This
finding suggests that a few nerve fibers remain capable of stimulation
even when ENoG shows total nerve degeneration. In most cases, the
nerve conduction block is localized between the geniculate ganglion
and the IAC segments of the facial nerve. Failure to generate a motor
unit potential when the tympanic segment of the nerve is stimulated
indicates that the nerve is 100% degenerated, or that the conduction
block is more distal. If the nerve appears normal in the tympanic
portion, although there is edema and erythema of the IAC segment,
total degeneration should be suspected. If erythema and edema are
apparent in the tympanic segment, a mastoid decompression is added.

Preoperative preparation
The risks of middle fossa decompression of the facial nerve are
discussed with the patient, which include cerebrospinal fluid leak (4%
to 6%), infection (1%), hearing loss (1%), dizziness (1%), intracranial
hemorrhage (<1%), and aphasia (<1%). When the decision is made to
proceed with surgical decompression, the procedure should be
performed as soon as possible. Appropriate preoperative laboratory
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 and imaging studies are obtained, along with a Stenvers projection
plain radiograph of the temporal bone to identify the floor of the middle
cranial fossa and superior semicircular canal. Cefazolin, mannitol, and
dexamethasone are given before the skin incision and are continued for
48 hours postoperatively.

General anesthesia and transoral endotracheal intubation are

accomplished; thereafter, the bed is rotated 180 degrees for access (
Fig. 26.3 ). Paralytic agents must be reversed before the skin incision. A
urinary catheter is placed to monitor fluids and diuresis. The hair is
shaved approximately 10 cm above and 5 cm behind the ear. The entire
side of the head and face are prepared, and EMG needles placed in the
orbicularis oculi and oris muscles ( Fig. 26.4A ) for facial nerve
monitoring. A clear drape is placed over the prepared area to allow
visualization of the entire side of the face in the case of monitoring
equipment failure ( Fig. 26.4B ). Intraoperative auditory brainstem-
evoked recording is not routinely performed.

Fig. 26.3

Operating room setup for middle cranial fossa approach.

Fig. 26.4

(A) Electrode placement for intraoperative electromyography. (B) Draping with exposure of
half the face for visual monitoring of facial movement.

Surgical Technique
The skin incision is marked as shown in Fig. 26.5 and carried down to
the level of the temporalis fascia. Meanwhile, mannitol (0.5 g/kg body
weight) and hyperventilation (partial pressure of CO 2 of <30 mm Hg)
are initiated by the anesthesiologist to relax the brain. After the
posteriorly based skin flap is elevated, a 4 × 6 cm piece of temporalis
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 fascia is harvested and set aside in a moist gauze for use at the time of
closure. An anteriorly based, inferiorly staggered muscle flap is
elevated down to the level of the linea temporalis and reflected forward
with an Adson cerebellar retractor. Staggering the incisions prevents
dural exposure if wound dehiscence occurs. The zygomatic root
identifies the floor of the middle cranial fossa and is the central
landmark of the craniotomy. The skin and muscle flaps should be
wrapped with moist sponges and secured with temporary retraction
sutures.

Fig. 26.5

Skin incision for middle cranial fossa approach. Mastoid exposure can be obtained by
extending incision postauricularly. The incision of the anteriorly based temporalis muscle
flap is offset to keep suture lines from being directly in line.

The craniotomy should be approximately 4 cm in the anteroposterior

dimension and 5 cm cephalocaudal ( Fig. 26.6A ). The anteroposterior
margins must be kept parallel to ensure the stability of the middle
cranial fossa retractor. The craniotomy can be created with either
cutting burs or a craniotomy saw. The bone flap should be elevated
with care by using a blunt dural elevator. Occasionally, the middle
meningeal artery is embedded within the bone, requiring bipolar
coagulation to free it. The bone flap is wrapped in moist gauze and set
aside until closure.

Fig. 26.6

(A) Craniotomy for middle cranial fossa exposure. Inferior expansion of the craniotomy
allows more exposure during dural elevation. The vertical margins must be parallel for
stability of the retractor. The craniotomy should be centered on the temporal root of the
zygoma (dashed line) . (B) The placement of the House-Urban middle cranial fossa
retractor.

Dural elevation from the floor of the middle cranial fossa is

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 accomplished with a Freer or Joker elevator, always in a posterior-to-
anterior direction, which prevents injury to the greater superficial
petrosal nerve and geniculate ganglion. The petrous ridge is identified
at the posterior margin of the craniotomy, and the dura slowly elevated
over the arcuate eminence and meatal plane. The dural reflections are
cauterized and sharply transected to allow elevation to the anterior
petrous ridge. The hiatus of the facial canal with the greater superficial
petrosal nerve and artery is the anterior margin of elevation. Further
anterior elevation exposes the foramen spinosum and the pterygoid
venous plexus, which can cause troublesome oozing throughout the
procedure.

After dural elevation, cottonoid sponges can be placed at the anterior

and posterior margins of the elevation to help retract the dura during
placement of the self-retaining middle cranial fossa retractor ( Fig.
26.6B ).

Before the bony exposure of the facial nerve, the Stenvers projection
radiograph or coronal CT scan is reexamined to determine the depth of
the superior semicircular canal in the temporal bone. The superior
semicircular canal is the first structure to be located. When its blue line
is identified, the remaining intratemporal structures have consistent
anatomical locations. The landmarks of the middle cranial fossa floor
can be quite subtle. The arcuate eminence may not be apparent and, in
many instances, is not parallel with the superior semicircular canal. One
consistent anatomical feature to remember is that the plane of the
superior semicircular canal is almost always perpendicular to the
petrous ridge ( Fig. 26.7 ). If the arcuate eminence is not initially
apparent, drilling is begun posterior to the semicircular canal, slowly
removing the tegmen mastoideum with a moderate-sized diamond bur.
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 The whitish color of the membranous temporal bone can be
distinguished from the yellow, dense otic capsule bone of the superior
canal. When the superior canal is identified, drilling in a parallel
direction with the canal gradually exposes the blue line.

Fig. 26.7

Exposure of the superior semicircular canal blue line and position of internal auditory canal
(IAC) 60 degrees anterior to a line through the blue line. The superior canal blue line is
almost always perpendicular to the petrous ridge.

When the location of the superior canal is confirmed, an anterior line 60

degrees to the blue line locates the position of the IAC. The depth of
the IAC varies, but drilling medially near the petrous ridge provides a
safe route to the canal. Drilling laterally near the anterior ampulla of the
superior semicircular canal places the geniculate ganglion, labyrinthine
segment of the facial nerve, and cochlea at risk. When the blue line of
the IAC is exposed, bone is removed in a lateral direction until the
vertical crest is found ( Fig. 26.8 ). The bone can now be removed over
the geniculate ganglion and tegmen tympani.

Fig. 26.8

(A to D) Middle cranial fossa exposure of CN VII and surrounding anatomy. Bone is removed
from the tegmen tympani to expose the tympanic segment of CN VII. Note the edema of the
internal auditory canal segment of CN VII, frequently found in Bell’s palsy. SSC , Superior
semicircular canal.

The labyrinthine segment of the facial nerve is the narrowest portion of

the fallopian canal and lies in an anterosuperior plane from the vertical
crest to the geniculate ganglion. A 1-mm diamond bur is used to
remove the bone over the labyrinthine segment, while the area directly
anterior to the segment is closely observed for the blue line of the basal
turn of the cochlea. The final layer of bone is removed from the
labyrinthine, geniculate, and proximal tympanic segments of the facial
:
 nerve with thin, angled hooks and blunt microelevators. At this point,
marked swelling of the nerve in the IAC, labyrinthine segment,
geniculate ganglion, and proximal tympanic segments is usually
observed. Further swelling is apparent after neurolysis. A disposable
microscalpel (Beaver No. 59-10) is used to slit the periosteum and
epineural sheath.

Intraoperative EMG is used to localize the region of the nerve

conduction block. Direct stimulation of the most distal exposed
tympanic segment of the nerve is performed with monopolar or bipolar
microforceps ( Fig. 26.9 ). If the conduction block is medial to the point
of stimulation, and the nerve not completely degenerated, a motor unit
potential is observed. Stimulating more medially toward the IAC fails to
elicit a motor unit potential if the conduction block is at the MF.

Fig. 26.9

Intraoperative evoked electromyography to identify the site of the nerve conduction block.
If the conduction block is medial to the geniculate ganglions, stimulation of the tympanic
segment results in motor unit potential (1); stimulation of internal canal segment (3) results
in no response. The conduction block is usually at the meatal foramen (MF). LSC , Lateral
semicircular canal; SSC , superior semicircular canal; SVN , superior vestibular nerve.

Upon completion of the decompression and confirmation of the site of

the conduction block, the opened IAC is covered with a piece of
temporalis muscle. The previously harvested temporalis fascia is
placed over the opened floor of the middle fossa after bone waxing the
opened mastoid air cells. The dural retractor is removed, and the
anesthesiologist is asked to reestablish a normal partial pressure of
carbon dioxide.

A corner of the craniotomy bone flap is harvested and placed superior

to the fascia to prevent herniation of the temporal lobe dura into the
:
 attic and IAC. The temporal lobe is allowed to reexpand into the middle
cranial fossa floor. The remainder of the craniotomy flap is placed on
the dura and the temporalis closed, creating a watertight seal with
interrupted absorbable sutures. The skin is closed with a deep layer of
interrupted absorbable sutures and an outer layer of nylon
nonabsorbable sutures. A mastoid dressing is applied and no drains are
used.

Postoperative Care
Postoperative care includes observation in the intensive care unit
overnight, limitation of fluids (1500 to 1800 mL/day), dexamethasone
(8 mg every 8 hours for 48 hours), cefazolin (2 g every 12 hours for 48
hours), routine neural checks, and limitation of analgesia to codeine.
There is little postoperative pain, and narcotics stronger than codeine
may mask intracranial complications. The patient is transferred to a
routine postoperative floor the next morning, encouraged to begin
ambulation, and started on a diet as tolerated. On postoperative day 3,
and daily thereafter, observations for cerebrospinal fluid rhinorrhea are
made by asking the patient to lean forward with the head between the
knees. If cerebrospinal fluid rhinorrhea occurs, a spinal drain must be
placed for 4 to 5 days. Following this regimen, only very rarely has a
patient required surgical closure of the leak. Patients are usually
discharged from the hospital on postoperative days 3 to 5. No
intracranial complications, including intracranial hemorrhage, aphasia,
or seizures, occurred in the Iowa series.

Limitations and special considerations

Dural elevation can be difficult, especially in patients older than 65
:
 years. If a dural tear occurs, a temporalis fascia repair must be
performed. Hearing loss can occur from contact of the rotating bur with
an intact ossicular chain or by entrance into the cochlea or labyrinth.
Vestibular dysfunction can occur in a similar fashion. If the
membranous labyrinth is violated, immediate placement of a small
amount of bone wax may preserve the auditory and vestibular function.

Correct positioning of the craniotomy and maintaining parallel vertical

margins are essential. Meticulous hemostasis must be maintained with
bipolar cautery, oxidized cellulose, and pressure. A dry surgical field is
crucial for microscopic dissection of subtle landmarks and prevention
of complications. If large apical air cells are opened, they must be
plugged with temporalis muscle to prevent cerebrospinal fluid leakage.

In appropriately selected patients, facial nerve decompression offers a

significant benefit for maximizing facial nerve outcomes. The middle
fossa approach is technically challenging, and the anatomy of the
middle cranial fossa floor is variable and presents some difficulty in
identification of landmarks. The surgeon must have precise knowledge
of the three-dimensional anatomy of the temporal bone. Many hours in
the temporal bone dissection laboratory are required to attain the
delicate microsurgical skills necessary for this type of surgery. For
patients with severe facial nerve paresis or complete paralysis who can
tolerate middle fossa surgery and desire to proceed with surgical
intervention, facial nerve decompression should be offered. Referral to
a medical center with expertise in middle fossa surgery is warranted if
these services are not available to the patient.

The American Academy of Otolaryngology—Head and Neck Surgery

released guidelines for the management of Bell’s palsy in 2013. The
guidelines committee could not make a recommendation on whether
:
 decompression of the facial nerve was of value in Bell’s palsy. This
decision was made on the “nonrandomized clinical trials and the
equilibrium of the benefit and the harm.” They continued stating that,
“although the data supporting surgical decompression are not strong,
there may be a significant benefit for a small subset of patients who
meet eligibility criteria and desire surgical management.” There were
major differences in opinion on the committee regarding surgical
decompression. This difference of opinion derived from controversy
regarding the strength of evidence (C-level evidence vs. D-level
evidence) and ultimately low confidence in the evidence resulted in the
downgrade of surgical decompression to aggregate level D evidence.

Unfortunately, it will be very difficult to accumulate the necessary

subject population to complete a randomized control study on an
orphan-like disease patient population that would meet the criteria for
surgical decompression. The Gantz et al. study required 15 years to
accumulate the patient population reported in their study.

A letter to the editorial in Otology and Neurotology by de Ru et al.

addresses this issue very succinctly. They state,

For many practitioners of evidence-based medicine, it is easy to

devalue a decompression study, not double-blind randomized, long
inclusion period, varying groups, etc. However, what kind of a study
does one actually expect with regard to such a rare topic? Rare,
because the group with such a severe degree of nerve failure
rendering decompression an option is very small indeed. When
considering the usefulness of evidence, the quality of the medical
content and clinical relevance are at least of equal importance to the
quality of the methodology. When confronted with rare cases, one
should not jump to generalized conclusions. The above leads to the
:
 conclusions that (1) although all evidence is equal, some evidence is
more equal than other, and (2) a decompression can in certain
cases, when performed by a skilled surgeon, lead to a better
outcome then the conservative attitude. More research in carefully
selected centers is necessary to establish further conclusive
evidence.

Three separate reports using similar measures to select patients for

decompression of the facial nerve in Bell’s palsy suggest that the
procedure is of value when it is limited to those with severe Wallerian
degeneration, measured with the combination of ENoG and voluntary
EMG and surgical decompression and including the MF, labyrinthine
segment, and geniculate ganglion. , ,

Summary
Bell’s palsy is a clinical entity encountered with relative frequency by
practitioners of many specialties. Before making the diagnosis of Bell’s
palsy, other causes of facial paralysis must be excluded through
thorough history-taking and physical examination. Bell’s palsy and
Ramsay Hunt syndrome seem to be due to viral etiologies and seem to
benefit from medical therapy with steroids and antiherpetic
medications.

Electrodiagnostic testing in cases of Bell’s palsy with complete

paralysis is indicated and provides crucial information to guide surgical
decision-making and patient counseling. In cases of Bell’s palsy with
greater than 90% degeneration on ENoG and absence of voluntary
motor unit potentials on EMG, middle fossa craniotomy with
decompression of the labyrinthine, geniculate, and proximal tympanic
segments of the nerve should be offered to patients without medical
:
 contraindications to an intracranial procedure within 14 days of
symptom onset. Familiarity with the anatomy of the middle cranial fossa
is essential for effective decompression of the facial nerve and
avoidance of complications. Finally, a subgroup of idiopathic recurrent
facial paralysis can also benefit from decompression of the facial nerve
medial to the geniculate ganglion.

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