Sudden Hearing Loss

By Tim Hain, MD
Last modified 10/2012
Soha N. Ghossaini, MD, is assistant professor in the Department of Otolaryngology Head and
Neck Surgery at Columbia University College of Physicians and Surgeons, New York
Presbyterian Hospital, Columbia Center.

What is Sudden Hearing Loss?

What Causes Sudden Hearing Loss?

How is Sudden Hearing Loss Diagnosed?

How is Sudden Hearing Loss Treated?

Rehabilitation of patients with persistent hearing loss

Research Studies in Sudden Hearing Loss

References

What is Sudden Hearing Loss?

Sudden hearing loss (SHL) is defined as greater than 30 dB hearing reduction, over at least
three contiguous frequencies, occurring over a period of 72 hours or less. Some patients
describe that the hearing loss was noticed instantaneously in the morning and others report
that it rapidly developed over a period of hours or days. The severity of the hearing loss
however varies from one patient to another and only one ear is usually affected. Sudden
hearing loss frequently involves both ears (Schreiber et al 2010). Tinnitus is usually reported
in patients with SHL loss and vestibular symptomsare present in roughly 40% of cases
(Mattox & Simmons 1977). The incidence of SHL has been reported to be 5-30 per 100,000
person per year (Nosrati-Zarenoe et al 2007, Wu et al 2006) and accounts for 1% of all
sensorineural hearing loss cases (Hughes et al 1996). Males are equally affected as females.
The average age at onset is reported to be 46 to 49 years with increasing incidence with age
(Byl 1984).

What Causes Sudden Hearing Loss?

There are many causes for sudden hearing loss which include infectious, circulatory, inner ear
problems like menieres disease, neoplastic, traumatic, metabolic, neurologic, immunologic,
toxic, cochlear, idiopathic (unknown cause) and other causes. Unfortunately, even after a
thorough search for a possible pathology, the cause of sudden hearing loss remains unknown
in most patients (Hughes et al 1996).

How is Sudden Hearing Loss Diagnosed?

Evaluation usually begins with a careful history and physical examination looking for
potential infectious causes such as otitis media, systemic diseases and exposure to known
ototoxic medications. In essence, SHL is diagnosed by documenting a recent decline in
hearing. This generally requires an audiogram. Blood studies are usually performed in an
attempt to rule potentially systemic causes of SHL including syphilis, Lyme disease,
metabolic, autoimmune, and circulatory disorders. Magnetic resonance imaging (MRI) of the
brain is recommended to rule out an acoustic neuroma which is reported to be existent up to
15% of patients with sudden hearing loss (Aarnisalo et al 2004).

How is Sudden Hearing Loss Treated?

Due to the lack of a definite cause of sudden hearing loss, its treatment has been
controversial. Over the years, this has included systemic steroids, antiviral medications,
vasodilators, carbogen therapy either (alone or in combination) or no treatment at all.
The no treatment option was based on the high reported rate of spontaneous recovery up to
two third of cases (Cekin et al 2009).
Oral corticosteroid therapy is among the few treatment modalities that that have gained
acceptance and proved to be effective in selected studies and most importantly when
compared to placebo in 2 randomized controlled trials (Moskowitz et al 1984, Wilson et al
1980). On a different level, and in a retrospective study by Chen et al. in 2003, oral steroids

were proved to be effective in the treatment of SHL. The literature is inconsistent however
regarding the dose and the duration of treatment of oral steroids used in the treatment of SHL
within the same study or across different studies.
A recent study (Battaglia et al 2008) indicated that a combination of high-dose prednisone
taper (HDPT) in addition to intratympanic dexamethasone (IT-Dex) therapy may improve
hearing recovery. Another recent study showed a non-statistical difference in hearing
recovery for oral vs. intratympanic steroid treatment (Rauch et al 2011).
The effectiveness of hyperbaric oxygen treatment in SHL either as a primary, adjunct or as a
secondary therapy in SHL treatment failures has not been conclusively established in the
literature. Although some studies have shown improvement in hearing after hyperbaric
oxygen treatment (Fattori et al 2001, Narozny et al 2004) the lack of randomized control
trials makes it difficult to draw any conclusion (Horn et al 2005),
Antivirals seem reasonable, given the frequency that herpes family viruses have been
associated with SHL. In an animal study, combination treatment with an antiviral (acylovir)
and steroids reduced damage in animals whose ears were inoculated with herpes simplex
virus type 1 (HSV-1), compared to treatment with either acyclovir or prednisolone alone
(Stokroos et al 1999). Unfortunately, in humans, antiviral (like acyclovir or valacyclovir)
treatment when studied in randomized controlled studies did not add any benefit to steroid
treatment alone (Tucci et al 2002, Uri et al 2003, Westerlaken et al 2007). In addition these
medications will unlikely be of help when the cause is a virus that is not in the herpes family,
and one rarely knows at the time of the hearing loss which if any virus is responsible. In a
survey of 104 ENT physicians, %50 reported using antiherpetic therapy despite lack of
efficacious

evidence

(Conlin

&

Parnes

2007,

Shemirani

et

al

2009).

Vasodilators:
Several vasodilators have been tried with mixed results (Fetterman et al 1996, Kronenberg et
al 1992, Wang et al 2012). To date the effectiveness of vasodilators on SHL is not well
established in the literature.A recent meta-analysis concerning SHL and vasodiolators is
available: Wang and associates (2010).

Rehabilitation of patients with persistent hearing loss:

Sudden hearing loss could result in variable degrees of hearing handicap. Patients most
commonly report difficulty of hearing people sitting on their deaf side and difficulty hearing
in background noise. The rehabilitation of patients after SHL depends on the degree of the
resultant hearing loss and ranges from no intervention to the use of hearing aids and other
assistive listening devices. In patients with resultant severe to profound sensorineural hearing
loss however, regular and other powerful hearing aids might not be an option. In the past,
rehabilitation of such a group of patients was limited to the use of contralateral routing of
signal (CROS) hearing aid with reported mixed satisfaction, and most patients were left
unaided. Currently the bone anchored cochlear stimulator (BAHA system) offers an
alternative to the CROS system and was found to be effective in patients with unilateral
severe to profound sensorineural hearing loss and to provide a greater perceived benefit when
compared to the CROS hearing aid (Wazen et al 2003).

Research Studies in Sudden Hearing Loss

Intratympanic steroid therapy is being currently used in patients where systemic steroids are
contraindicated or in patients who fail to respond to oral steroids steroids with mixed results
(Herr & Marzo 2005, Slattery et al 2005). In this procedure, steroids are perfused or injected
into the middle ear and absorbed into the inner ear via the round window membrane.
Theoretically, when used intratympanically, the concentration of the drug at its site of action
(inner ear) will be higher and its side effects will be minimized.
Incomplete response to oral steroids is not well understood and is speculative. One of many
possible reasons is inability to reach adequate levels of steroids in the inner ear with
conventional oral steroid treatment. Animal studies have shown a higher perilymph (inner ear
fluid) concentration of steroids when installed in the middle ear as compared to their systemic
use (Parnes et al 1999). However, a recent study showed only mild improvements for a group
of patients treated via steroid perfusion who had initially failed to recover with systemic
treatment (Haynes et al 2007).
Clinically, the success rate of Intratympanic steroid therapy in patients with SHL is variable
in the literature and the available studies are limited to retrospective and non-controlled
prospective ones. In those studies steroids were used in various concentrations, regimens and

delivery methods and their effectiveness have not been established due to the lack of
randomized controlled trials. There have been some studies in the literature that discussed the
effectiveness of Intratympanic steroid therapy as a salvage mode of therapy in patients who
failed to respond to oral steroids (Herr & Marzo 2005, Slattery et al 2005).
Randomized controlled trials are needed to better establish the effectiveness of Intratympanic
steroid therapy in the treatment of patients with SHL. Currently a randomized controlled trial
is being initiated by the author at the New York Presbyterian Hospital of Columbia and
Cornell New York NY in order to evaluate the effectiveness of Intratympanic steroid therapy
in patients with SHL and to compare it to the more standard method of treatment, oral
steroids.
In conclusion, very few placebo controlled studies have been performed of treatment of SHL.
For this reason, there is presently a limited ability to determine what the optimal treatment of
SHL is. At the American Hearing Research Foundation (AHRF), we are interested in funding
good research on this condition. We have funded basic research on similar conditions in the
past. Learn more about donating to American Hearing Research Foundation (AHRF).

Sudden Deafness
On this page:

What is sudden deafness?

What causes sudden deafness?

How is sudden deafness diagnosed?

How is sudden deafness treated?

What research does the NIDCD support on sudden deafness?

Where can I find additional information about SSHL?

What is sudden deafness?

Sudden sensorineural hearing loss (SSHL), commonly known as sudden deafness, occurs as
an unexplained, rapid loss of hearingusually in one eareither at once or over several
days. It should be considered a medical emergency. Anyone who experiences SSHL should
visit a doctor immediately. Sometimes, people with SSHL put off seeing a doctor because
they think their hearing loss is due to allergies, a sinus infection, earwax plugging the ear
canal, or other common conditions. However, delaying SHHL diagnosis and treatment may
decrease the effectiveness of treatment.
Nine out of ten people with SSHL lose hearing in only one ear. SSHL is diagnosed by
conducting a hearing test. If the test shows a loss of at least 30 decibels (decibels are a
measure of sound) in three connected frequencies (frequency is a measure of pitchhigh to
low), the hearing loss is diagnosed as SSHL. As an example, a hearing loss of 30 decibels
would make conversational speech sound more like a whisper.
Many people notice that they have SSHL when they wake up in the morning. Others first
notice it when they try to use the deafened ear, such as when they use a phone. Still others
notice a loud, alarming "pop" just before their hearing disappears. People with sudden
deafness often become dizzy, have ringing in their ears (tinnitus), or both.
About half of people with SSHL will recover some or all of their hearing spontaneously,
usually within one to two weeks from onset. Eighty-five percent of those who receive
treatment from an otolaryngologist (a doctor, sometimes called an ENT, who specializes in
diseases of the ears, nose, throat, and neck) will recover some of their hearing.
Experts estimate that SSHL strikes one person per 5,000 every year, typically adults in their
40s and 50s. The actual number of new cases of SSHL each year could be much higher
because the condition often goes undiagnosed. Many people recover quickly and never seek
medical help.
Top

What causes sudden deafness?

Only 10 to 15 percent of the people diagnosed with SSHL have an identifiable cause. The
most common causes are:

Infectious diseases
Trauma, such as a head injury

Autoimmune diseases such as Cogans syndrome

Ototoxic drugs (drugs that harm the sensory cells in the inner ear)

Blood circulation problems

A tumor on the nerve that connects the ear to the brain

Neurologic diseases and disorders, such as multiple sclerosis

Disorders of the inner ear, such as Mnires disease.

Top

How is sudden deafness diagnosed?

To diagnose SSHL, a doctor will use a hearing test called pure tone audiometry. This test
helps him or her to determine if the hearing loss is caused by sound not reaching the inner ear
(because of an obstruction such as fluid or ear wax) or by a sensorineural deficit (because the
ear isnt processing the sound that reaches it). Pure tone audiometry can also show the range
of hearing thats been lost.
If you are diagnosed with sudden deafness, your doctor will probably order other tests to try
to determine an underlying cause for your SSHL. These tests may include blood tests,
imaging (usually magnetic resonance imaging, or MRI), and balance tests.
Top

How is sudden deafness treated?

The most common treatment for sudden deafness, especially in cases where the cause is
unknown, is corticosteroids. Steroids are used to treat many different disorders and usually
work by reducing inflammation, decreasing swelling, and helping the body fight illness.
Steroids are usually prescribed in pill form. In recent years, direct injection of steroids behind
the eardrum into the middle ear (from here the steroids travel into the inner ear), called
intratympanic corticosteroid therapy, has grown in popularity. In 2011, a clinical trial
supported by the NIDCD showed that intratympanic steroids were no less effective than oral
steroids, but were less comfortable overall for patients. They remain an option for people who
cant take oral steroids.
Additional treatments may be needed if your doctor discovers an actual underlying cause of
SSHL. For example, if your SSHL is caused by an infection, your doctor may prescribe
antibiotics. If youre taking drugs known to be toxic to the ear, your doctor may tell you to

stop or switch to another drug. If you have an autoimmune condition that causes your
immune system to attack the inner ear, you may need to take drugs to suppress your immune
system.

Top

What research does the NIDCD support on sudden

deafness?
Since so little is known about the causes of most cases of SSHL, researchers are studying
how changes in the inner ear, such as disrupted blood flow or inflammation, may contribute
to hearing loss. Researchers are also testing new ways to use imaging to help diagnose SSHL
and potentially detect its causes.
Top

Where can I find additional information about SSHL?

The NIDCD maintains a directory of organizations that provide information on the normal
and disordered processes of hearing, balance, taste, smell, voice, speech, and language.
Use the following keywords to help you search for organizations that can answer questions
and provide information on SSHL:

Brain injury
Late-deafened adults

Noise-induced hearing loss

Background
Acoustic neuromas are intracranial, extra-axial tumors that arise from the Schwann cell
sheath investing either the vestibular or cochlear nerve. As acoustic neuromas increase in
size, they eventually occupy a large portion of the cerebellopontine angle. Acoustic neuromas
account for approximately 80% of tumors found within the cerebellopontine angle. The
remaining 20% are principally meningiomas. In rare cases, a facial nerve neuroma, vascular
tumor, lipoma, or metastatic lesion is found within the cerebellopontine angle.

This table shows the distribution of presenting

symptoms, ie, the symptom that brought the patient to a physician and that
constituted the patient's chief ailment.

History of the Procedure

Over the last 80-90 years, the operative mortality rate has dropped dramatically from 40% at
the beginning of the century to less than 1% in the last decade. Postoperative facial paralysis,
once the rule, is now an uncommon permanent sequelae of acoustic tumor surgery. Attempts
at hearing conservation, unimaginable at the beginning of the 20th century, are increasingly
successful.
These very dramatic improvements are the result of the convergence of several factors. Vastly
improved imaging techniques permitting early diagnosis, adaptation of the microscope to the
operating theater, development of facial and auditory nerve monitoring techniques, improved
anesthesia, and improved perioperative management have all contributed to improved
outcomes.

Epidemiology

Frequency
Clinically diagnosed acoustic neuromas occur in 0.7-1.0 people per 100,000 population. The
incidence may be rising, a reflection of the increasing frequency with which small tumors are
being diagnosed with the more widespread use of MRI. A 2005 study by Lin et al suggested
the prevalence of incidental acoustic neuromas to be 2 in 10,000 people. [1] Careful autopsy
studies can detect small vestibular schwannomas in a higher percentage of elderly patients,
which suggests that many acoustic neuromas never become clinically apparent.

Etiology
Most patients diagnosed with an acoustic neuroma have no apparent risk factors. Exposure to
high-dose ionizing radiation is the only definite environmental risk factor associated with an
increased risk of developing an acoustic neuroma. Multiple studies have determined cell
phone use is not associated with an increased risk of developing an acoustic neuroma,
although data on the effects of long-term cell phone use are still pending.
Neurofibromatosis type II occurs in individuals who have defective tumor suppressor gene
located on chromosome 22q12.2. The defective protein produced by the gene is called merlin
or schwannomin. Bilateral acoustic tumors are a principle clinical feature of
neurofibromatosis type II, although other manifestations, including peripheral
neurofibromata, meningioma, glioma, and juvenile posterior subcapsular lenticular opacities,
are often present as well. Peripheral neurofibromatoma and cafe au lait spots, however, are
much less frequently observed than is typical in neurofibromatosis type I. Many patients with
neurofibromatosis type II present in late adolescence or early adulthood but occasionally may
present later in the fifth to seventh decade with slowly growing tumors.

Pathophysiology
The vast majority of acoustic neuromas develop from the Schwann cell investment of the
vestibular portion of the vestibulocochlear nerve. Less than 5% arise from the cochlear nerve.
The superior and inferior vestibular nerves appear to be the nerves of origin with about equal
frequency. Overall, 3 separate growth patterns can be distinguished within acoustic tumors, as
follows: (1) no growth or very slow growth, (2) slow growth (ie, 0.2 cm/y on imaging
studies), and (3) fast growth (ie, 1.0 cm/y on imaging studies). Although most acoustic
neuromas grow slowly, some grow quite quickly and can double in volume within 6 months
to a year.
Although some tumors adhere to one or another of these growth patterns, others appear to
alternate between periods of no or slow growth and rapid growth. Tumors that have
undergone cystic degeneration (presumably because they have outgrown their blood supply)
are sometimes capable of relatively rapid expansion because of enlargement of their cystic
component. Because acoustic tumors arise from the investing Schwann cell, tumor growth
generally compresses vestibular fibers on the surface. Destruction of vestibular fibers is slow;
consequently, many patients experience little or no disequilibrium or vertigo. Once the tumor
has grown sufficiently large to fill the internal auditory canal, it may continue growth either
by expanding bone or by extending into the cerebellopontine angle. Growth within the
cerebellopontine angle is generally spherical.

Acoustic tumors, like other space-occupying lesions, produce symptoms by any of 4

recognizable mechanisms: (1) compression or distortion of the spinal fluid spaces, (2)
displacement of the brain stem, (3) compression of vessels producing ischemia or infarction,
or (4) compression and/or attenuation of nerves.
Because the cerebellopontine angle is relatively empty, tumors can continue to grow until
they reach 3-4 cm in size before they contact important structures. Growth is often
sufficiently slow that the facial nerve can accommodate to the stretching imposed by tumor
growth without clinically apparent deterioration of function. Tumors that arise within the
internal auditory canal may produce relatively early symptoms in the form of hearing loss or
vestibular disturbance by compressing the cochlear nerve, vestibular nerve, or labyrinthine
artery against the bony walls of the internal auditory canal.
As the tumor approaches 2.0 cm in diameter, it begins to compress the lateral surface of the
brain stem. Further growth can occur only by compressing or displacing the brain stem
toward the contralateral side. Tumors greater than 4 cm often extend sufficiently far
anteriorly to compress the trigeminal nerve and produce facial hypesthesia. As the tumor
continues to grow beyond 4 cm, progressive effacement of the cerebral aqueduct and fourth
ventricle occurs with eventual development of hydrocephalus.

Presentation
Unilateral hearing loss is overwhelmingly the most common symptom present at the time of
diagnosis and is generally the symptom that leads to diagnosis. Assume that any unilateral
sensorineural hearing loss is caused by an acoustic neuroma until proven otherwise. The
tumor can produce hearing loss through at least 2 mechanisms, direct injury to the cochlear
nerve or interruption of cochlear blood supply. Progressive injury to cochlear fibers probably
accounts for slow progressive neurosensory hearing loss observed in a significant number of
patients with acoustic neuromas. Sudden and fluctuating hearing losses are more easily
explained on the basis of disruption of cochlear blood supply.
Consistent with direct injury to cranial nerve VIII, a significant number of individuals with
acoustic neuroma have speech discrimination scores reduced out of proportion to the
reduction in the pure-tone averagea feature typical for retro-cochlear lesions. This can
often be demonstrated through audiological testing by a phenomenon called "rollover," in
which speech discrimination scores decrease as the volume of the speech stimulus increases.
Such marked reductions in speech discrimination scores are not invariable, however. A
normal speech discrimination score does not rule out an acoustic tumor. Patients with
acoustic tumors may have normal or near-normal hearing and speech discrimination scores.
Hearing loss associated with acoustic neuroma can be sudden or fluctuating in 5-15% of
patients. Such hearing loss may improve spontaneously or in response to steroid therapy.
Consequently, a gadolinium enhanced MRI should be ordered in anyone with a sudden or
fluctuating loss even if hearing returns to normal.
Not surprisingly, the discovery of acoustic neuromas in persons with normal hearing has been
increasing as gadolinium-enhanced MRI is becoming more common. In addition, tumor size
poorly correlates with hearing status as patients with large tumors may have normal hearing
and patients with small tumors may be profoundly deaf in the affected ear. The presence of

unilateral tinnitus alone is a sufficient reason to evaluate an individual for acoustic tumor.
Although tinnitus is most commonly a manifestation of hearing loss, a few individuals with
acoustic tumors (around 10%) seek treatment for unilateral tinnitus without associated
subjective hearing loss.
Vertigo and disequilibrium are uncommon presenting symptoms among patients with acoustic
tumors. Rotational vertigo (the illusion of movement or falling) is uncommon and is
occasionally seen in patients with small tumors. Disequilibrium (a sense of unsteadiness or
imbalance), on the other hand, appears to be more common in larger tumors. Overall, if
carefully questioned, approximately 40-50% of patients with an acoustic neuroma report
some balance disturbance. However, balance disturbance is the presenting symptom in less
than 10% of patients. The destruction of vestibular fibers apparently is sufficiently slow as to
permit compensation.
Headaches are present in 50-60% of patients at the time of diagnosis, but fewer than 10% of
patients have headache as their presenting symptom. Headache appears to become more
common as tumor size increases and is a prominent feature in patients who develop
obstructive hydrocephalus associated with a very large tumor.
Facial numbness occurs in about 25% of patients and is more common at the time of
presentation than facial weakness. Objective hypoesthesia involving the teeth, buccal
mucosa, or skin of the face is associated with larger tumors, but a subjective reduction in
sensation that cannot be documented on objective examination occurs commonly with
medium-sized and small tumors. Decrease in the corneal reflex generally occurs earlier and
more commonly than objective facial hypoesthesia. Although approximately 50-70% of
individuals with large tumors have objectively demonstrable facial hypoesthesia, they are
often unaware of it, and it is uncommonly the presenting symptom.
The motor fibers in the facial nerve can accommodate very substantial stretching as long as it
occurs slowly and are much more resistant to injury than sensory fibers of the trigeminal
nerve. Facial weakness is sufficiently uncommon (< 1%) that facial weakness associated with
a small- or medium-size tumor should raise suspicion that it is not an acoustic neuroma.
Other diagnosis should be considered including facial neuroma, hemangioma, meningioma,
granuloma, arteriovenous malformation (AVM), or lipoma. Large tumors (>4 cm) can
obstruct the flow of spinal fluid through the ventricular system by distorting and obstructing
the fourth ventricle. In the early decades of this century, 75% of patients presented with
hydrocephalus.

Indications
Treatment depends on multiple factors including the age and medical status of the patient,
tumor size and location, hearing status, and patient preference. In older patients with small
tumors, careful observation may be elected consisting of serial MRIs. In older patients with a
growing tumor, radiosurgery may be an appropriate option. Young patients, large tumors
(greater than 2.5 to 3 cm) and patients with small tumors and intact hearing may choose
surgery. See Surgical therapy.

Relevant Anatomy

The cerebellopontine angle is a space filled with spinal fluid. It has the brain stem as its
medial boundary, the cerebellum as its roof and posterior boundary, and the posterior surface
of the temporal bone as its lateral boundary. The floor of the cerebellopontine angle is formed
by the lower cranial nerves (IX-XI) and their surrounding arachnoid investments. The
flocculus of the cerebellum may lie within the cerebellopontine angle and may be closely
associated with cranial nerves VIII and VII as they cross the cerebellopontine angle to enter
the internal auditory canal.
The facial nerve arises 2-3 mm anterior to the root entry zone of the vestibulocochlear nerve.
The foramen of Luschka (ie, the opening of the lateral recess of the fourth ventricle) is
located just inferior and posterior to the root entry zones of the facial and vestibulocochlear
nerve. A tuft of choroid plexus can frequently be observed extruding from it. Inferior and a bit
anterior to the foramen of Luschka is the olive, and just posterior to the olive lie the rootlets
of origin for cranial nerves IX, X, and XI. The hypoglossal nerve exits the brain stem through
a series of small rootlets anterior to the olive.

Vascular structures within the cerebellopontine angle

The most important vascular structure within the cerebellopontine angle is the anterior
inferior cerebellar artery (AICA). It arises most commonly as a single trunk from the basilar
artery but can arise as 2 separate branches. In rare cases, it originates as a branch of the
posterior inferior cerebellar artery (PICA). As the AICA moves from anterior to posterior, it
first follows the ventral surface of the brain stem, but within the cerebellopontine angle it
takes a long loop laterally to the porus acousticus. In 15-20% of cases, the AICA actually
passes into the lumen of the internal auditory canal before turning back on itself toward the
posterior surface of the brain stem. The AICA can thus be divided into the premeatal, meatal,
and postmeatal segments.
The main branch of the AICA passes over cranial nerves VII and VIII in only 10% of cases.
The remainder of the time, it either passes below the VII and VIII cranial nerves or, in 2550% of individuals, actually passes between them. Three branches that regularly arise from
the meatal segment of the AICA can be identified. Small perforating arteries supply blood to
the brain stem. The subarcuate artery passes through the subarcuate fossa into the posterior
surface of the temporal bone, and the third regular branch is the internal auditory artery
(labyrinthine artery). Cranial nerves VII and VIII receive their blood supply from small
branches of AICA.
Two venous structures must be kept in mind during surgical procedures involving the
cerebellopontine angle. The petrosal vein (of Dandy) brings returning venous blood from the
cerebellum and lateral brain stem to the superior or inferior petrosal sinus. It is generally
encountered in the area of the trigeminal nerve anterior to the porus acousticus. The petrosal
vein often carries enough venous blood that its obstruction can lead to venous infarction and
cerebellar edema, and it should be preserved if at all possible. Additional venous blood
reaches the superior petrosal sinus through a series of bridging veins that cross the
cerebellopontine angle. Although every attempt should be made to preserve these veins, their
sacrifice is generally inconsequential.
The vein of Labb carries returning venous blood from the inferior and lateral surface of the
temporal lobe to the superior petrosal sinus, tentorial venous lakes, or the transverse sinus. Its
configuration and anatomy is quite variable. However, obstruction, obliteration, or occlusion

of the superior petrosal sinus may, in some cases, result in occlusion of the vein of Labb.
Sudden occlusion of the vein of Labb carries with it high risk of venous infarction of the
temporal lobe and rapid life-threatening cerebral edema.

Nerves
The facial nerve leaves the brain stem anterior to the foramen of Luschka. As it leaves the
brain stem, the fibers are sheathed in oligodendroglia derived from the central nervous
system. Within a few millimeters of leaving the brain stem, however, the nerve loses its
oligodendroglial ensheathment and becomes ensheathed instead by Schwann cells.
Throughout the remainder of its peripheral course, it remains within its Schwann cell
investment. It passes directly across the cerebellopontine angle for about 15 mm,
accompanied by the vestibulocochlear nerve. It consistently enters the internal auditory canal
by crossing the anterior superior margin of the porus acusticus.
The vestibulocochlear nerve arises from the brainstem slightly posterior to the facial nerve. It
remains sheathed in oligodendroglia for approximately 15 mm (almost to the point at which it
passes into the internal auditory canal). It has the longest oligodendroglial investment of any
peripheral nerve. The junction between oligodendroglia and Schwann cells (ie, the
Obersteiner-Redlich zone) occurs just medial to the porus acousticus. Because acoustic
neuromas arise from Schwann cells, they arise most commonly within the most lateral
portions of the cerebellopontine angle or the internal auditory canal.
The nervus intermedius (nerve of Wrisberg) leaves the brain stem together with the
vestibulocochlear nerve. At some point within the cerebellopontine angle, the nervus
intermedius crosses over to become associated with the facial nerve. It may do so as several
separate rootlets. The point where the nervus intermedius crosses to become associated with
the facial nerve shows considerably variation, but in 22% of individuals, it is adherent to the
vestibulocochlear nerve for 14 mm or more. As the vestibulocochlear and facial nerve reach
the porus acousticus (medial opening of the internal auditory canal) they pass together with
the nervus intermedius and sometimes a loop of AICA.

Internal auditory canal

The internal auditory canal is approximately 8.5 mm in length (range 5.5-10.5 mm), lined
with dura, and filled with spinal fluid. Its medial end is oval in shape and is referred to as the
porus acousticus. Its lateral end is a complicated structure referred to as the fundus or lamina
cribrosa. The fundus is divided into a superior and inferior half by the transverse crest. The
upper half is further subdivided into an anterior and posterior segment by a vertical crest,
often referred to as Bills Bar, named after William House, who popularized its importance as
a surgical landmark. The vertical crest separates the macula cribrosa superior, a series of very
small openings through which the terminal fibers of the vestibular nerve pass in order to
reach the cupula of the superior semicircular canal, from the meatal foramen, which marks
the point at which the facial nerve leaves the internal auditory canal and enters the fallopian
canal as the labyrinthine segment.
Because the most lateral portion of the internal auditory canal is 4-5 mm inferior to the level
of the geniculate ganglion, the labyrinthine segment of the facial nerve must take a vertically
oriented course upward to reach it. The labyrinthine segment may be less than a millimeter
wide as it passes between the cochlea and the anterior end of the superior semicircular canal.

The inferior portion of the fundus is a single oval-shaped space, the anterior portion of which
is occupied by a rounded depression (tractus spiralis foraminosus) filled with small openings
to accommodate the terminal branches of the cochlear nerve. The posterior portion is filled
with a macula crista inferior through which pass the terminal ends of the inferior vestibular
nerve.

Temporal bone
The anatomy of the superior surface of the temporal bone must be mastered if middle fossa
approaches are to be undertaken successfully. Laterally, the irregular superior surface of the
temporal bone transitions relatively smoothly to the temporal squamosa. The free edge of the
tentorium and the superior petrosal sinus attach to the medial edge of the superior surface of
the temporal bone. The arcuate eminence, a bony prominence that is perpendicular to the
petrous ridge and lies two centimeters medial to the squamous temporal bone, often overlies
the superior semicircular canal. The arcuate eminence is often difficult to identify, especially
in well-pneumatized temporal bones.
The geniculate ganglion generally lies within the substance of the temporal bone just medial
to and a few millimeters anterior to the head of the malleus. The geniculate ganglion may be
dehiscent, or alternatively, it may lie several millimeters beneath the superior surface of the
bone. The head of the malleus is generally easy to identify if the thin bone of the tegmen
tympani is removed so as to enter into the middle ear space. In difficult surgical situations,
the head of the malleus can be used to identify the geniculate ganglion. The greater
superficial petrosal nerve originates from the geniculate ganglion and courses anteromedially,
passing over the superior surface of the temporal bone at the facial hiatus. The facial hiatus is
generally 4-8 mm anterior to the geniculate ganglion. The greater superficial petrosal nerve
can generally be identified in this area. It can then be followed retrograde to the geniculate
ganglion.
The middle meningeal artery and associated veins traverse the foramen spinosum, which is
located approximately 1 cm anterolaterally to the greater superficial petrosal nerve. The
mandibular division of the trigeminal nerve traverses the foramen ovale, which lies a few
millimeters anterior and medial to the foramen spinosum. The horizontal portion of the
carotid canal courses through the anterior temporal bone medial to the foramen spinosum and
foramen ovale. The cochlea cannot be identified from the surface appearance of the superior
temporal bone. It lies just anterior and inferior to the labyrinthine segment of the facial nerve
but is deep to the geniculate ganglion.

Contraindications
Few absolute contraindications to the surgical removal of an acoustic tumor exist. Serious
medical illness may make surgical removal in some patients too risky. Surgery must often be
performed for large tumors with brainstem shift and obstructive hydrocephalus, even in the
presence of significant medical illness. The translabyrinthine approach is contraindicated in a
patient with chronic otitis media.
The decision to operate should be carefully considered when the tumor is within the internal
auditory canal of a patient's only hearing ear. In some cases, observing the tumor until

hearing has been lost is best, while in other cases, attempting surgical removal with hearing
conservation is more prudent.

Imaging Studies

The definitive diagnostic test for patients with acoustic tumors is

gadolinium-enhanced MRI.
o Well-performed scanning can demonstrate tumors as small as 1-2
mm in diameter. On the other hand, thin-cut CT scanning can miss
tumors as large as 1.5 cm even when intravenous contrast
enhancement is used.
o

Gadolinium contrast is critical because nonenhanced MRI can miss

small tumors.

Fast-spin echo techniques do not require gadolinium enhancement

and can be performed very rapidly and relatively inexpensively.
However, such highly targeted techniques risk missing other
important causes of unilateral sensory hearing loss, including intraaxial tumors, demyelinating disease, and infarcts.

MRI is contraindicated in individuals with ferromagnetic implants.

Fine-cut CT scanning of the internal auditory canal with contrast can rule
out a medium-size or large tumor but cannot be relied upon to detect a
tumor smaller than 1-1.5 cm.

If suspicion is high and MRI is contraindicated, air-contrast cisternography

has high sensitivity and can detect relatively small intracanalicular tumors.

Diagnostic Procedures

A variety of audiometric tests were developed in the middle of the century

in an attempt to identify patients with increased likelihood of having an
acoustic neuroma. That was a worthwhile undertaking when definitive
radiographic
imaging
consisted
of
some
form
of
either
pneumoencephalography or formal arteriography. Such testing is no
longer used. Even the auditory brainstem evoked response (ABR) is now
infrequently used as a screening test for acoustic neuroma. ABR screening
techniques miss 20-35% of acoustic tumors smaller than 1 cm. Moreover,
ABR is likely to miss those tumors in patients with excellent hearing, which
are the cases most favorable for hearing conservation procedures.

Histologic Findings
Two histologic types of tissue have been identified in acoustic tumors. Antoni A tissue
consists of elongated spindle cells with a palisading pattern. Antoni B tissue, on the other
hand, has a loose spongy texture and markedly reduced cellularity. A given acoustic neuroma
may contain areas with both Antoni A and Antoni B tissue. Another histologic feature
characteristic of schwannomas are rows of palisading nuclei called Verocay bodies. Although
the histologic appearance of acoustic tumors is fairly straightforward, they can occasionally
be difficult to distinguish from meningiomas. Immunohistochemical staining can distinguish

schwannomas from meningiomas in difficult cases. Schwannomas are immunoreactive to S100 antibody while meningiomas are immunoreactive to epithelial membrane antibody
(EMA).

Staging
As a rule, acoustic neuromas are benign tumors, although rare cases of malignant acoustic
neuromas have been reported in the literature. No widely accepted staging system exists for
acoustic neuromas.

Medical Therapy
Acoustic neuromas are managed in one of the following 3 ways: (1) surgical excision of the
tumor, (2) arresting tumor growth using stereotactic radiation therapy, or (3) careful serial
observation.

Observation
Simple observation without any therapeutic intervention has been used in the following
groups of patients:

Elderly patients
Patients with small tumors, especially if their hearing is good

Patients with medical conditions that significantly increase the risk of

operation

Patients who refuse treatment

Patients with a tumor on the side of an only hearing ear or only seeing eye
o

In a number of series reported to date, the individuals who are

being observed ultimately require therapeutic intervention in
between 15-40%.

During an observation period, most (70% or more) patients who are

eligible for hearing conservation surgery initially lost their eligibility.

Telian has analyzed the important variables that should be

evaluated when observation is considered, and these include the
following:[2] 1) preoperative hearing in both ears, 2) the risk of
immediate hearing loss as a consequence of surgery, 3) the risk of
facial nerve paralysis, 4) the risk of other surgical complications and
their seriousness, 5) the patient's life expectancy, 6) the size of the
tumor, 7) tumor growth rate, and 8) patients with neurofibromatosis
type 2 (NF2) or bilateral tumors.

Stereotactic radiotherapy
Stereotactic radiotherapy has emerged within the last 20 years as an alternative to
microsurgery for selected patients with acoustic neuroma.

Stereotactic radiation therapy makes use of one of several radiation

sources and is administered using a variety of different machines with
proprietary names (eg, Gamma Knife, CyberKnife, BrainLAB).
Stereotactic therapy uses radiation delivered to a precise point or series of
points to maximize the amount of radiation delivered to target tissues
while minimizing the exposure of adjacent normal tissues. It can be
delivered as a single dose or as multiple fractionated doses.

The effects of radiation delivered at the current low dose likely prevents
further tumor growth by causing obliterative endarteritis of the vessels
supplying the tumor. Radiosurgery may affect tumor cells undergoing
mitosis by causing double strand DNA breaks. Hansen et al demonstrated
acoustic neuroma cells are radioresistant at the current low-dose radiation
used with radiosurgery.[3]

Comparison of microsurgery and stereotactic radiation is difficult for the

following reasons:

Tumor size is inconsistently reported in the literature.

Data using the lower radiation dosages are available for only the
past 10 years.

Because the goal of radiotherapy is control of tumor growth,

understanding whether posttreatment neuroimaging reflects
adequate treatment or merely the natural history of vestibular
schwannomas is difficult.

No data concerning the risk for secondary tumor induction by

radiotherapy are available.

Advantages of radiation therapy include the following:

o

Decreased length of stay

Decreased cost

Rapid return to full employment

Lower immediate posttreatment morbidity and mortality

Disadvantages of stereotactic radiation include the following:

o

Necessity for regular monitoring and frequent rescanning (In the

end, costs associated with long-term monitoring could exceed those
of surgery.)

Does not eliminate the tumor and may fail to control tumor growth,
sometimes requiring salvage surgery.

Higher incidence of trigeminal nerve injury.

Unknown long-term incidence of secondary malignancies. The best

current estimates of developing a secondary malignancy from the
radiosurgery are 1 in a 1000 patients over 30 years.

Does not address disequilibrium and may lead to long-term balance

dysfunction.

Fractionated stereotactic radiotherapy provides very good tumor control of acoustic neuroma,
but it also carries a risk of the patient developing hydrocephalus. It is necessary before
treatment to closely monitor patients at high risk (ie, those with larger tumors with partial
effacement of the fourth ventricle) and to monitor them more closely during follow-up.
Before tumor diameter grows to larger than 2 cm, it would be beneficial to offer treatment to
patients with progressive acoustic neuroma while the risk of hydrocephalus is low.[4]
Stereotactic radiosurgery and fractionated stereotactic radiotherapy have the potential for
hearing preservation, at least in the short-term. Hearing preservation is dependent on multiple
factors including tumor size, tumor location, and radiation dose. Most centers use a dose of
12-13 Gy at the 50% isodose line when considering hearing preservation. Hearing
preservation is also dependent on the radiation dose to the cochlea, cochlear nerve, and
cochlear nucleus. Kim et al recently noted transient volume expansion that is commonly seen
after radiosurgery portends the worse prognosis for hearing preservation.[5]

Surgical Therapy
Surgical removal remains the treatment of choice for tumor eradication. Various surgical
approaches can be used to remove acoustic tumors. Each approach is discussed in detail in
the following sections.

Preoperative Details
Three different approaches are used in the management of acoustic neuromas, the
retrosigmoid, translabyrinthine, and middle fossa approaches. All have advantages and
disadvantages as indicated below.

Advantages of the retrosigmoid approach

The retrosigmoid approach can be applied to all acoustic tumors and to

many other histologic tumor types. It can be used for operations that
sacrifice hearing and operations that attempt to conserve hearing. Its only
limitation in this respect is its inapplicability for small tumors that occupy
the far-lateral portions of the internal auditory canal.
The retrosigmoid approach provides the best wide-field visualization of the
posterior fossa. The inferior portions of the cerebellopontine angle and the
posterior surface of the temporal bone anterior to the porus acusticus are
much more clearly observed than via the translabyrinthine approach.
Panoramic visualization is especially helpful when displacement of nerves
is not predictable, which occurs commonly with meningiomas.
Hearing conservation surgery can be attempted even for relatively large
tumors via the retrosigmoid approach. Destruction of the labyrinth is not
required as part of the retrosigmoid approach.

Disadvantages of the retrosigmoid approach

The retrosigmoid approach may require cerebellar retraction or resection.

Manipulation of the cerebellum provides opportunities for postoperative
edema, hematoma, infarction, and bleeding.
Increased incidence of cerebrospinal fluid leak occurred in some series.

The retrosigmoid approach is associated with greater likelihood of severe

protracted postoperative headache.

The highest incidence of tumor recurrence or persistence occurs with

retrosigmoid approaches.

Advantages of the translabyrinthine approach

The translabyrinthine approach provides the best view of the lateral brain
stem facing the acoustic tumor.
Retraction of the cerebellum is almost never necessary.

The fundus and lateral end of the internal auditory canal are completely
exposed; the facial nerve can be identified at a location where it is
undistorted by tumor growth and compressed into the labyrinthine
segment, decreasing the risk of delayed postoperative facial nerve palsy.

Incidence of cerebrospinal fluid leak is decreased in some series.

If the facial nerve has been divided or sacrificed, the translabyrinthine

approach may allow restoration of the facial nerve continuity by rerouting
the facial nerve and performing a primary anastomosis. Consequently,
interposition graft can sometimes be avoided.

Facial function is more frequently preserved in some series.

Disadvantages of the translabyrinthine approach

Hearing sacrifice is complete and unavoidable.

The inferior portions of the cerebellopontine angle and cranial nerves are
not as well visualized as they are in the retrosigmoid approach. The
temporal bone anterior to the porus acusticus is also less well visualized.

A fat graft is required. Removal of fat from the abdomen creates

opportunities for donor site complications, including hematoma, bleeding,
and infection.

The sigmoid sinus is more vulnerable to injury. Bleeding from the sigmoid
sinus can be difficult to control and can significantly increase operative
blood loss. If a dominant sigmoid sinus is occluded during the operation,
postoperative intracranial pressure elevation or venous infarct can occur.

A high jugular bulb or anteriorly placed sigmoid sinus can substantially

compromise the space available for tumor removal. Occasionally, the
space is so contracted that another approach has to be selected.

Advantages of the middle cranial fossa approach

It is the only procedure that fully exposes the lateral third of the internal
auditory canal without sacrificing hearing.
It is extradural.

Disadvantages of the middle cranial fossa approach

The facial nerve generally courses across the anterior superior portion of
the tumor. Consequently, it is in the way during tumor removal and is
more vulnerable to injury. Although long-term facial nerve outcomes are as

good with the middle cranial fossa approach as with other approaches,
temporary postoperative paresis is more common.
The risk of dural laceration and avulsion becomes increasingly more likely
as patients become older. The dura mater in elderly patients is more
friable. This becomes especially noticeable during the sixth and seventh
decades of life.

The approach provides only very limited exposure of the posterior fossa.

The operation is technically difficult and demanding.

Some patients incur postoperative trismus related to manipulation and/or

injury to the temporalis muscle.

The temporal lobe must be retracted, presenting the opportunity for

temporal lobe injury, usually in the form of a hematoma that is
asymptomatic and, therefore, probably occurs more frequently than is
realized. Scattered reports exist of seizure disorder following middle
cranial fossa surgery, presumably due to temporal lobe injury.

Approach Selection
A variety of different considerations go into deciding which approach should be used for any
individual patient. These variables are detailed below.

Preoperative hearing level

If the patient has no useful hearing, either the translabyrinthine or the retrosigmoid approach
is selected, depending upon the experience and training of the surgeon. In most centers
performing large numbers of surgeries for acoustic tumors, the translabyrinthine approach is
preferred. Opinions vary considerably about what constitutes useful hearing. The 50/50 rule
is frequently quoted. The rule suggests that individuals with a pure-tone average greater than
50 dB and speech discrimination less than 50% do not have useful or salvageable hearing.
Other surgeons have stricter criteria and consider only individuals with better than a 30-dB
pure-tone average and more than 70% discrimination for hearing conservation operations.

Auditory brainstem response

Normal preoperative ABR findings favor hearing conservation. Marked abnormalities of
ABR wave morphology or increased wave I-III and I-V latencies make hearing conservation
less feasible.

Electronystagmography
An abnormal caloric test on electronystagmography (ENG) increases the likelihood of
successful hearing conservation surgery. The ENG tests the horizontal semicircular canal,
which is innervated by the superior vestibular nerve. A normal ENG finding arguably
demonstrates that the superior vestibular nerve is normal. Consequently, the acoustic tumor
must have originated from the inferior vestibular nerve, which is directly adjacent to the
cochlear nerve. Surgical removal, then, is more likely to directly injure the cochlear nerve or
interfere with cochlear blood supply. Vestibular evoked myogenic potential (VEMP) testing is
abnormal when the inferior vestibular nerve is affected. As a result, an abnormal VEMP with

normal caloric testing on ENG strongly suggests an inferior vestibular nerve tumor with
poorer hearing preservation.

Tumor size
Opportunities for hearing conservation decrease as tumors become larger. Hearing is much
more difficult to conserve when tumors are 1.5-2.0 cm in diameter than if they are small
intracanalicular tumors. Consequently, some surgeons limit hearing conservation surgery to
smaller tumors, preferring to use a translabyrinthine approach to maximize the chance of
facial nerve conservation for larger tumors.

Tumor position
If hearing conservation is to be attempted and the tumor lies within the lateral portions of the
internal auditory canal, many surgeons prefer a middle fossa approach. The middle fossa
approach permits direct exposure of the lateral end of the internal auditory canal without
sacrificing hearing. The approach is frequently used for any tumor lying completely within
the internal auditory canal, although tumors limited to the medial portions of the internal
auditory canal can be managed using a retrosigmoid approach. Some surgeons extend the use
of the middle fossa technique to include tumors that extend as much as 0.5-1.0 cm into the
cerebellopontine angle. Division of the superior petrosal sinus may be required to gain
sufficient access to the posterior fossa with larger tumors.
Generally, however, tumors that have significant volume medial to the plane of the porus
acousticus are extirpated using a retrosigmoid approach if hearing is to be conserved. If
hearing conservation is not an issue, the retrosigmoid approach is sometimes preferred for
tumors with significant inferior extension since the lower cranial nerves are better visualized
with a retrosigmoid approach. Occasionally, the retrosigmoid approach is combined with a
translabyrinthine approach for such large acoustic neuromas.

Relevant anatomy
The following anatomic variations can make the translabyrinthine approach much more
difficult and at times impossible.

High-riding jugular bulb: In some individuals, the jugular bulb may actually
ride up above the level of the inferior internal auditory canal.
Anteriorly placed sigmoid sinus: In such circumstances, the distance
between the sigmoid sinus and the external auditory canal may be a few
millimeters or less. Such a dramatic limitation of the space within which
the surgeon has to operate not only makes a successful tumor extirpation
much more difficult but puts the facial nerve and the displaced sinus itself
at significantly increased risk of injury.

Contracted sclerotic mastoid: Such mastoid cavities provide little room for
tumor removal. Moreover, they are often associated with suppurative otitis
media, in itself a contraindication to the translabyrinthine approach.

Reduced or absent flow in the contralateral sinus: Previous operation,

trauma, congenital anomalus development, and previous or concurrent
disease can all result in markedly reduced or absent venous outflow

through the contralateral sinus. In such cases, consideration may be given

to a retrosigmoid approach merely because it reduces the risk of injury to
the remaining sinus, occlusion of which would result in catastrophic
venous infarction.

Surgeon preference
Some surgeons have more experience and are much more comfortable with one approach
relative to another. Generally, such preferences should be followed. However, if hearing
conservation is a realistic option using an approach unfamiliar to the primary surgeon,
consideration should be given to referring the patient to someone who is familiar with the
appropriate approach.

Patient preference
Patient preferences should be carefully considered even when they do not conform to the
surgeon's judgment. Some patients are adamant about going to any lengths for hearing
conservation even when the treating physician is quite convinced that the patient's hearing is
so poor as to be of little or no practical utility. Some patients willingly sacrifice even good
hearing if doing so even slightly enhances the possibility of successful facial nerve
preservation. Some patients have very clear-cut opinions about one type of incision versus
another (sometimes based on cosmetic consideration).

Intraoperative Details
Translabyrinthine approach
The translabyrinthine approach is the most versatile of the 3 common approaches to the
cerebellopontine angle. The main disadvantage is profound deafness in the operated ear due
to violation of the membranous labyrinth. In general, even the largest acoustic neuromas can
be removed through a translabyrinthine craniotomy. In addition, the facial nerve is found at
the fundus of the internal auditory canal where the vertical crest (Bills bar) provides a natural
plane for facial nerve dissection from the superior vestibular nerve. At the authors institution,
the translabyrinthine approach is preferred with any acoustic neuroma over 2 cm or in an ear
with poor hearing.
The patient is laid supine and a Mayfield head frame may be used. An incision is then made
two finger-breadths from the postauricular sulcus. The temporalis muscle and mastoid
periosteum are identified. The skin flap is then elevated anteriorly, leaving as much
periosteum down as possible. The periosteum is then incised along the linea temporalis and
then towards the mastoid tip in a T-shaped fashion. This will allow a water-tight second layer
for closure to prevent postoperative cerebrospinal fluid leakage. The mastoid periosteum is
then elevated from the underlying mastoid bone. Often, the emissary vein is encountered and
this can be controlled with bipolar coagulation and/or bone wax.
A wide cortical mastoidectomy is performed. The middle and posterior fossa dura are
identified as well as the sigmoid sinus. The bone is removed from these structures to allow
retraction of the temporal lobe dura and sigmoid sinus. Next, the antrum, lateral semicircular
canal, and vertical facial nerve are identified.

The incus is removed and a facial recess is performed. The in tensor tympani tendon is
sectioned and the eustachian tube is packed with oxidized cellulose packing. The middle ear
space is then packed with temporalis muscle.
A labyrinthectomy is performed and the jugular bulb is identified. The internal auditory canal
is subsequently identified and troughs are developed both superiorly and inferiorly around the
internal auditory canal until approximately 270 of internal auditory canal is exposed. The
remaining bone is then removed from the internal auditory canal and the facial nerve is found
as it turns into the labyrinthine segment. The superior vestibular nerve is then followed out to
the ampullated end of the superior semicircular canal.
At this point, the transverse crest and vertical crest (Bills bar) are identified. The superior
vestibular nerve is then reflected inferiorly from the ampullated end of the superior
semicircular canal. The facial nerve can often be found superior medial to this and is
confirmed using a facial nerve stimulator. At this point, the tumor is generally debulked and
the facial nerve is located at the origin from the brain stem. Once the tumor is adequately
debulked, the acoustic neuroma is then dissected from the facial nerve. Often, the facial nerve
is very adherent to the acoustic neuroma around the porus of the internal auditory canal.
Once the tumor has been removed, the posterior fossa dura is then re-approximated. Fat is
harvested from the abdomen and packed into the surgical defect. The periosteal and skin
layers are closed in a water-tight fashion. The patient wears a pressure dressing for 3 days.

Retrosigmoid approach
The patient may be placed in the supine position on the operating table and with the head
toward the contralateral shoulder. The true lateral or park-bench position is still used by some
surgeons because it permits the occiput to be rotated a little bit more superiorly. This allows a
slightly more direct view of the internal auditory canal.
The operation is performed through either a vertically oriented linear incision or an anteriorly
based U-shaped flap. An occipital craniotomy is then performed. Any mastoid air cells are
carefully waxed off to prevent postoperative cerebrospinal fluid leak. The dura is opened and
the arachnoid incised. The cerebellum frequently falls away from the posterior surface of the
temporal bone after the cisterna magna has been opened. Hyperventilation, steroids, and
intraoperative diuretics (principally mannitol) are used to reduce intracranial pressure and to
provide additional exposure with a limited amount of retraction. Nonetheless, gentle
cerebellar retraction is occasionally required especially in larger tumors.
Once adequate exposure has been obtained, the tumor is clearly visualized along with the
brain stem and lower cranial nerves. However, cranial nerves VII and VIII are rarely
observed because they are almost always pushed forward and lie across the anterior surface
of the tumor, which cannot be visualized. Debulking of the tumor is the next step and must be
carefully performed so as to maintain the anterior portions of the capsule in order to prevent
injury to cranial nerve VII and/or VIII. Once the tumor has been substantially debulked, the
posterior wall of the internal auditory canal can be removed using a high-speed drill.
Great care must be taken to avoid injuring the labyrinth while removing the posterior wall of
the internal auditory canal. Portions of the labyrinth quite commonly are medial to the lateral
end of the internal auditory canal. Although no single anatomic landmark is completely

reliable for prevention of injury to the labyrinth, the singular nerve and its canal, and the
operculum of the vestibular aqueduct, are used as important surgical landmarks. Careful
measurements taken from preoperative CT scans can provide useful information during
drilling of the posterior wall of the internal auditory canal.
The length of the internal auditory canal varies considerably, and knowing exactly how much
posterior canal wall needs to be removed to adequately expose the tumor can help limit
inadvertent injury to the labyrinth. Blind extraction of tumor from the internal auditory canal
without removing the posterior wall poses a significant risk to the facial and/or auditory nerve
integrity and increases the chance of leaving tumor at the fundus. Use of intraoperative
angled endoscopes has been reported as an adjunct in performing this phase of the operation.
Every effort should be made to prevent bone dust from entering the subarachnoid space
during the intradural drilling of the internal auditory canal. One probable cause for severe and
intractable postoperative headache is spillage of bone dust into the subarachnoid space during
tumor removal. Surgicel, Gelfoam, Telfa pads, and/or cottonoid strips are placed around the
operative site so that bone dust adheres to them and is removed as they are removed. Once
the internal auditory canal is exposed, the dura is opened and the tumor is removed. Although
never proven, dissection from medial to lateral is thought to be less traumatic to both the
cochlear nerve and to the vascular supply of the inner ear. The vestibular nerves are generally
sacrificed, and unless hearing is to be preserved, the cochlear nerve is sacrificed as well.
Eventually, the surgeon is left with the anterior portions of the capsule adhered to the brain
stem and cranial nerve VII. As the tumor capsule is carefully removed from the brain stem,
the root entry zone of cranial nerve VII can be identified. The capsule is then carefully
removed from the facial nerve with as little trauma as possible.
The facial nerve monitor facilitates this portion of the dissection. A meaningful amount of
data now shows that results are improved when facial nerve monitoring is employed. A
variety of techniques have been used to monitor the cochlear nerve when hearing
preservation is desired. The most commonly used method is intraoperative ABR, but it has a
number of disadvantages. Most importantly, it requires summing a large number of
repetitions in order to extract a response from background noise. Consequently, a delay
occurs between surgical manipulations and ABR changes. Direct cochlear nerve monitoring
offers the advantage of real-time feedback, but a fully satisfactory method of placing and
securing the electrode still is lacking.
Once tumor removal is complete and hemostasis is absolute, the dura is closed and the
craniotomy defect is repaired, either by replacing the original bone flap or with
methylmethacrylate or hydroxyapatite.

Middle cranial fossa approach

Although some surgeons use an extended middle cranial fossa approach for tumors that
extend a centimeter or more outside the porus acusticus into the cerebellopontine angle, the
middle cranial fossa approach is most frequently used for intracanalicular tumors. It is, by
consensus, the approach of choice for small tumors that lie within the lateral portions of the
internal auditory canal when hearing conservation is desired.

The head must be in the true lateral position. In young individuals with a supple neck, this
can often be accomplished by turning the head to the side with the patient in the supine
position. But if neck mobility is limited or concern exists that forced head turning will limit
posterior fossa circulation or aggravate cervical spine disorders, then a true lateral (parkbench) position should be used.
Exposure must be centered over a vertically oriented line that passes approximately 1 cm
anterior to the external auditory meatus. This is most easily accomplished through a linear
incision. A posteriorly based U-shaped or curvilinear S-shaped incision can be used if
concern exists about scar contracture. Depending upon the incision used, the temporalis
muscle is incised or reflected inferiorly. A temporal craniotomy (approximately 5 cm by 5
cm) is performed with its base at the root of the zygoma. The dura is elevated from the floor
of the middle cranial fossa, and osmotic diuretics, head elevation, hyperventilation, and
steroids are used to limit cerebral edema.
The dura of the temporal lobe is then elevated off the superior surface of the temporal bone.
The anterior extent of such elevation is usually the foramen spinosum, but the middle
meningeal artery can be divided between clips and elevation continued anteriorly to the
foramen ovale if additional exposure is desired. Dural elevation should proceed from
posterior to anterior to avoid injury to an exposed greater superficial petrosal nerve or
geniculate ganglion. Bleeding from the veins associated with the middle meningeal artery is
often quite brisk but can generally be controlled with oxidized cellulose packing. Medial
dissection continues to the free edge of the temporal bone.
The superior petrosal sinus is attached to the posterior surface of the temporal bone but not
always at its superior edge. Care must be taken to avoid injuring it. If inadvertent injury
occurs, bleeding can generally be controlled with intraluminal oxidized cellulose packing,
electrocautery, or hemoclips. When extended middle cranial fossa approaches are employed,
the superior petrosal sinus is deliberately divided between clips.
When it can be identified easily, the arcuate eminence is an extremely helpful landmark.
Careful drilling can often identify the blue line of the superior canal inferior to it. Because the
most difficult exposure to achieve during middle fossa surgery is the lateral posterior end of
the internal auditory canal, dissection is performed as close to the superior semicircular canal
as possible. The greater superficial petrosal nerve is generally easy to visualize and can be
followed retrograde to the geniculate ganglion. It lies approximately 1.0 cm directly medial to
the foramen spinosum. Once the area of the geniculate is identified, small diamond burrs are
used to completely expose it. If the greater superficial petrosal nerve cannot be located and no
other landmarks are available, the middle ear space can be entered from above and the head
of the malleus can be identified. The geniculate ganglion lies approximately 2-3 mm anterior
and medial to the head of the malleus.
Once the geniculate ganglion has been completely exposed, the labyrinthine portion of the
nerve can be identified and followed medially and inferiorly into the internal auditory canal.
The labyrinthine portion of the nerve takes a markedly vertical and medial course as it moves
from the lateral geniculate ganglion to the proximal fundus of the internal auditory canal,
which lies 5 or more millimeters deep to the geniculate ganglion. Some surgeons prefer to
identify the internal auditory canal medially. Once the medial end of the canal is completely
identified, they follow the canal laterally to the fundus of the internal auditory canal.

The bone overlying the internal auditory canal should be removed until approximately 270
of the internal auditory canal is exposed. The most difficult area to expose is the point at
which the superior vestibular nerve penetrates the labyrinthine bone to innervate the ampulla;
however, exposure in this area is critical if the anatomy of the lateral end of the internal
auditory canal is to be well visualized. If the superior vestibular nerve channel is identified,
tumor removal is generally successful and relatively straightforward.
Larger tumors frequently have the facial nerve splayed out over the anterior superior portions
of the tumor. Tumor removal begins, as with other approaches, by careful debulking. Once
the tumor is debulked, enough room is created within the internal auditory canal to carefully
remove the tumor capsule from the inferior surface of the facial nerve. Again, care must be
taken to avoid torsion or twisting of the nerve during tumor removal.
Once the tumor has been completely removed, the integrity of the facial nerve is tested using
the intraoperative facial nerve monitor. Presumably, the monitor has been in use throughout
the case. If the facial nerve can be stimulated with low stimulus intensities, chances of good
postoperative facial nerve function increase. Fat is then packed into the internal auditory
canal after using bone wax to fill obvious air cells to prevent postoperative cerebrospinal
fluid leak. The facial nerve monitor generally alerts the physician if fat is being packed in too
tightly that the integrity of the facial nerve is being compromised. Retractors are removed,
and the temporal lobe dura is allowed to relax. The bone plate is replaced using miniplates,
and the wound is closed in multiple layers.

Postoperative Details
Unless a complication develops, postoperative care is straightforward. The patient is
generally kept in the ICU overnight so that rapid intervention is available if postoperative
intracranial pressure increases or bleeding occurs. Vestibular rehabilitation should begin on
the first postoperative day and continues twice daily throughout the hospital stay. Most
patients can be discharged on the third or fourth postoperative day.

Follow-up
A follow-up MRI is obtained within 6-12 months after surgical excision to document the
completeness of tumor removal and to serve as a baseline for further follow-up scans.
Assuming complete tumor removal, follow-up MRI should be obtained at 5 years and at 10
years. If the findings on the 10-year scan are normal, further imaging should be performed
only if clinical circumstances require it. Postoperative MRI scans must be performed with fatsuppressed techniques if fat was used to obliterate the surgical site.

Complications
Arterial injury
Injury to the AICA (much less commonly to the PICA) fortunately occurs very rarely.
Although the AICA may be loosely attached to the tumor capsule, separating it from the
tumor is generally fairly easy. Sacrificing the AICA itself has variable consequences

depending upon the details of individual patient anatomy. It can be catastrophic and lead to
devastating neurologic injury or death.
The branches of AICA most vulnerable to injury are, of course, the labyrinthine artery and
branches supplying the facial nerve. Some otherwise perplexing cases of postoperative facial
nerve weakness may be related to interruption of facial nerve vascular supply due to
coagulation of small branches of the AICA. Failure to conserve hearing may be due to the
disruption of cochlear blood supply. Because the labyrinthine artery may be intimately
associated with the tumor, sacrifice often cannot be avoided. Conservation of the internal
labyrinthine artery becomes more difficult as tumor size increases, doubtlessly accounting in
some measure for the reduced success in hearing conservation with larger tumors. Neurologic
injury or cerebral edema secondary to venous injury usually occurs as a result of injury to the
sigmoid sinus itself, the petrosal vein of Dandy, or to the vein of Labb.
Occlusion of the sigmoid sinus has variable effects depending largely upon the patient's
unique venous anatomy. If the contralateral venous outflow tract is patent and communication
through the torcula herophili is adequate, complete occlusion may be asymptomatic. The size
of the 2 sigmoid sinuses is usually asymmetrical, with a greater volume of blood flowing
through the right-sided sinus. Depending on how much more blood flows through the
dominant sinus, occlusion of the dominant sinus can result in catastrophic increases in
intracranial pressure, venous infarction, and even death. Because a number of potential
collaterals exist between the torcula herophili and the jugular bulb, occlusion of the sigmoid
sinus close to the torcula herophili is much more likely to have significant adverse effects
than its occlusion close to the jugular bulb.
The petrosal vein of Dandy is a single large outflow tract in some patients but consists of
series of several large veins in others. Its occlusion can result in edema and infarction of
either the temporal lobe or the brain stem. Although neurologic injury secondary to occlusion
of the Dandy vein is not inevitable, severe injury can occur, and the petrosal vein should be
carefully preserved.
Occlusion of the vein of Labb results in severe edema of the temporal lobe and temporal
infarct. The edema can be sufficiently severe to cause brain herniation and death. The vein of
Labb generally enters the superior petrosal or transverse sinus between the torcula herophili
and the point at which the superior petrosal sinus joins the transverse sinus. Thus, it is
generally not directly in the field during acoustic tumor surgery. Occasionally, however,
injury to the superior petrosal sinus results in its obliteration, and in some instances, the vein
of Labb is also injured or obstructed. Its presence and importance should be kept in mind
during acoustic tumor surgery.
Hemorrhage into the posterior fossa in the immediate postoperative period can produce
brainstem compression and death quite rapidly. Death can occur within a few minutes. Rapid
neurologic deterioration in the first 24 hours postoperatively should raise suspicion of
posterior fossa hemorrhage and mandates rapid and decisive intervention. If time permits, a
rapid unenhanced CT scan should be obtained to secure the diagnosis while the operating
room is prepared for an immediate return to surgery. If neurologic deterioration is rapid,
forgo CT scanning and take the patient directly back to the operating theatre. If deterioration
is very rapid with loss of consciousness, decerebrate posturing, and signs of imminent death,
open the wound at the bedside to permit a posterior fossa decompression prior to emergent

transportation of the patient to the operating room for wound exploration, debridement, and
extensive irrigation.

Cerebellar injuries
Injury to the cerebellum was common in the early decades of the century, but its incidence
has dramatically diminished in recent decades. Cerebellar injuries still occur but are generally
not troublesome. The rotating shaft of the surgeon's burr is often the culprit because surgeons
usually look past the shaft to the head of the burr to concentrate on bone removal. The shaft is
often outside the surgical field of view. Such small areas of injury rarely have noticeable
sequelae. Bleeding can be controlled with oxidized cellulose, cautery, or gelatin sponges, and
edema is limited. Direct injury to the cerebellar hemisphere from compression and retraction,
intracerebral hemorrhage, infarction due to alteration of the arterial inflow, or venous
engorgement with our without infarction can produce severe edema of the entire cerebellum.
Brainstem compression and/or intracranial herniation can produce death. Obstruction of the
fourth ventricle and cerebral aqueduct can produce significant hydrocephalus.
Management should consist of aggressive use of osmotic diuretics, hyperventilation, and
steroids. If medical management is unsuccessful, resection of part of the involved cerebellar
hemisphere may be required.

Facial paralysis
In some cases, postoperative facial paralysis is unavoidable. The tumor may simply be
attached too intimately to the thin attenuated facial nerve. Sometimes the tumor has
enveloped the facial nerve, and tumor removal cannot be accomplished without resection of a
portion of the facial nerve.
Eye care is critical to successful management of postoperative facial paralysis. Make liberal
use of artificial tears specifically adapted to deal with dry eye (eg, Bion Tears). At night,
place ocular lubricants (eg, Lacri-Lube) in the eye. If aggressive use of artificial tears during
the day (q15-30min) and ointment at night is insufficient to maintain corneal hydration and
exposure keratitis begins to develop, then consider use of an eye patch, placement of a gold
weight, and lower lid shortening procedures. Tarsorrhaphy should be used only as a last resort
and is only very rarely required. Coexisting injury to cranial nerve V with corneal hypesthesia
or anesthesia vastly increases the problem in management. The lack of corneal sensation
provides the patient no reliable guide as to the severity of corneal epithelial disruption. In
such cases, tarsorrhaphy is much more likely to be required.

Cerebrospinal fluid complications

Transient abnormality of cerebrospinal fluid resorption may lead to mild temporary
postoperative hydrocephalus. Although postoperative shunting can facilitate controlling
cerebrospinal fluid fistula, it is now rarely, if ever required. Even when hydrocephalus is
present in the preoperative period, it generally resolves without difficulty in the first few
postoperative weeks.
Postoperative meningitis occurs in 2 forms. Bacterial meningitis is potentially life threatening
and occurs in less than 1% of patients in the postoperative period. It can occur within the first

24-36 hours postoperatively, or its appearance may be delayed for a couple of weeks. Once
initiated, it can progress very rapidly, and individuals can lapse from a normal level of
consciousness into a dense coma in a matter of a few hours.
Consequently, intervention must be rapid. Diagnosis depends upon the presence of fever and,
in the alert patient, the presence of headache, stiff neck, nuchal rigidity, and decreasing level
of consciousness. If meningitis is suspected, perform an immediate lumbar puncture to obtain
fluid for culture, but only after a CT scan has excluded the possibility of significant
hydrocephalus, which could lead to brain herniation.
Obtain spinal fluid for Gram stain, glucose, protein, and white blood cell count. If the Gram
stain is positive, spinal fluid glucose is less than 40 m/dL, or the spinal fluid white blood cell
count is higher than 2500 cells/mm 3, begin antibiotics immediately pending culture results. If
the spinal fluid does not meet any of these criteria, closely observe the patient with the
understanding that any deterioration of the condition requires a repeat lumbar puncture for
additional spinal fluid.
Aseptic meningitis has been reported in 7-70% of postoperative neurosurgical patients. It
shares with bacterial meningitis the clinical signs of increasing headache, fever, nuchal
rigidity, and elevation of cerebrospinal fluid pressure. Spinal fluid profile in such patients
shows marked elevation of white blood cell count and cerebrospinal fluid protein levels, but
cerebrospinal fluid glucose remains within the reference range, and culture results (when they
are finally complete) are normal. Corticosteroids are extremely helpful in managing aseptic
meningitis, and their prompt administration often results in marked decrease in headache and
nuchal rigidity within a few hours.
Spinal fluid leak through either the wound or the eustachian tube and middle ear occurs in 220% of patients. It can occur after translabyrinthine or retrosigmoid approaches and is less
common after middle fossa craniotomy. When it follows retrosigmoid approaches, the path of
egress is generally through pneumatized air cell tracts.
Cerebrospinal fluid is produced within the ventricular system at a rate of 0.3 mL/min or at
about 500 mL/day. It enters the subarachnoid space in the posterior fossa via the midline and
lateral foramen of the fourth ventricle. Contamination of the cerebrospinal fluid circulation
by blood, bone dust, and necrotic debris at the time of surgery often impairs cerebrospinal
fluid absorption directly by mechanical interference in the arachnoid villi or indirectly by
inciting an inflammatory response within the subarachnoid space. The syndrome may vary
from brief asymptomatic elevation of cerebrospinal fluid pressure to clinically manifested
aseptic meningitis (discussed above). Cerebrospinal fluid escaping through the wound can
initially be managed by resuturing the wound. Sometimes this results in elimination of the
difficulty, while at other times it merely produces cerebrospinal fluid rhinorrhea, as the spinal
fluid finds an alternate means of egress.
If the cerebrospinal fluid leak persists for more than 12-24 hours after initiation of
conservative management, including pressure dressing and consistent head elevation, then
consider reducing the cerebral spinal fluid pressure by 1 of 3 measures, including (1) multiple
lumbar punctures, (2) continuous or intermittent drainage via lumbar intradural catheter, or
(3) permanent cerebrospinal fluid diversion by means of an indwelling shunt.

When cerebrospinal fluid diversion is selected, the most common method is an indwelling
subarachnoid catheter placed into the lumbar subarachnoid space. The drain is opened
episodically so as to remove 200-400 mL of spinal fluid in any given 24-hour period. Some
surgeons observe a minimum drainage period of 2 days, others 5 days. General consensus is
that, if the drain has been in place for more than 5 days, it should be replaced to avoid
infection. Variation among surgeons is considerable as to when reexploration is required.
Some centers reexplore after 24-48 hours of drainage; other centers use as many as two 5-day
trials of continuous lumbar drainage before considering a second operation.
Severe postoperative headache has long been associated with retrosigmoid procedures. This
problem appears to have diminished considerably since the introduction of 2 intraoperative
steps: (1) great care is taken to avoid contaminating the spinal fluid and subarachnoid space
with bone dust, and (2) the bone flap is replaced and any residual bony defect is eliminated
with methylmethacrylate or hydroxyapatite. The latter step eliminates the direct attachment of
posterior cervical musculature to the dura. When postoperative headaches do occur, they
should be managed with relatively high-dose nonsteroidal anti-inflammatory agents and
aggressive regimens of manipulative physical therapy.

Outcome and Prognosis

Tinnitus
Tinnitus becomes worse in only 6-20% of individuals after tumor removal. In a substantial
number of individuals, the tinnitus remains unchanged. In about 25-60% of patients, tinnitus
is eliminated or improved. Although 30-50% of patients who had no preoperative tinnitus
develop it in the immediate postoperative period, such tinnitus only rarely becomes
troublesome.

Recurrence/residual tumor
Recurrence is uncommon after acoustic tumor removal. Overall, the recurrence rate is less
than 5%. The vast majority of recurrences follow retrosigmoid removal. Presumably, a small
amount of tumor is left in the lateral end of the internal auditory canal where intraoperative
visualization is difficult. Tumor recurrence may be suspected by recurring headache, altered
sensation to the face, or dysarthria and dysphasia if the lower cranial nerves become
involved.
Inflammation in the tumor bed may persist for months and even years after acoustic tumor
removal, and consequently, areas of contrast enhancement are present on postoperative
gadolinium MRI. Distinguishing tumor recurrence from postoperative inflammation can be
quite difficult. Tumor recurrences tend to be globular while postoperative inflammatory
enhancement tends to be linear. Often, however, one must view serial scans to detect tumor
recurrence. Fat suppression techniques are essential for postoperative surveillance to
distinguish recurrence from fat packing. Surveillance for postoperative tumor recurrence
should persist for 8-10 years postoperatively.

Facial function
Preservation of facial function continues to improve, especially with the widespread use of
facial nerve monitoring. However, facial nerve outcomes continue to vary according to tumor
size. When tumors are smaller than 1.5 cm, good facial nerve function can be expected
(House-Brackmann grade I-II) in more than 90% of patients.
In addition to tumor size, preoperative electrophysiologic testing can help predict
postoperative outcome, although this testing is not commonly used. Demonstrable
electrophysiologic abnormalities on nerve conduction studies, electromyography, and blink
reflex testing correlate well with postoperative facial nerve deficits. Arriaga has shown that
patients with poor facial nerve function at the time of discharge (House-Brackmann V-VI)
had a 25% chance of recovery of normal function (House-Brackmann I-II). Less optimistic is
the report of Sterkers. In his series of patients, anyone who had House-Brackmann III
function or worse at a 4- to 6-week postoperative evaluation was left with significant deficit
and generally had some synkinesis.
Facial nerve paralysis may be delayed and may develop within a few hours to a week or more
after acoustic neuroma removal. Incidence of delayed facial palsy varies from 10-30%. The
mechanism of action is unclear. Ischemia secondary to vasospasm, vascular injury, traction,
nerve edema, stretching, and even a viral reactivation have been proposed. Unlike final facial
nerve outcome, incidence of delayed facial paralysis does not appear to be related to tumor
size.
The vast majority of individuals who have delayed onset of facial paralysis make complete
and total recoveries. If deterioration is severe (more than 3 House-Brackmann grades), some
chance of poor long-term outcome exists. Perioperative steroids are widely used in an attempt
to enhance both immediate and long-term postoperative facial nerve function, but
unequivocal evidence for their effectiveness is lacking. The use of perioperative antiviral
agents is used by some centers to prevent delayed paralysis from viral reactivation, as in Bell
palsy.

Hearing outcome
The ability to preserve hearing has increased substantially over the last decade or two.
Depending on criteria for successful hearing conservation, hearing can be preserved in 3080% of properly selected patients.
Stereotactic radiation (the gamma knife) does not appear to have a significantly higher rate of
hearing conservation than does properly conducted surgery when long-term results are
compared. Chopra, et al demonstrated a hearing preservation rate of 44% at 10-year followup in 216 patients receiving Gamma Knife radiosurgery.
Rosenberg et al and Tucci et al have both shown reasonable stability of hearing over time
after surgery.[6] On the other hand, Shelton's study appears to show significant hearing
deterioration in 30-50% of patients who originally had successful hearing preservation.

Rehabilitation
The hearing deficit after the removal of an acoustic neuroma can have a significant impact on
quality of life. Rehabilitation options include a contralateral routing of signals (CROS)
hearing aid or more recently a bone anchored hearing aid (BAHA). The BAHA consists of a
surgical implanted titanium abutment that osseointegrates into the calvaria. A speech
processor is then snapped onto the abutment, allowing sound to transmit through the skull to
the normal contralateral ear.
In patients with neurofibromatosis type 2, all patients develop bilateral acoustic neuromas
and most will eventually lose hearing in both ears. The auditory brainstem implant (ABI) can
be inserted during a translabyrinthine craniotomy and provide patients the benefit of auditory
input to assist with communication.
If a patient experiences facial nerve weakness and not total paralysis after surgical removal,
often eye care consisting of artificial tears and lubricant will be sufficient until facial nerve
function returns. If the facial nerve is severed intraoperatively, the nerve can be approximated
at the time of surgery. If the patient has facial nerve paralysis 1 year after surgery, the chance
of further recovery is remote. At this time, a hypoglossal-facial nerve graft may be
considered. This will often result in improved tone and possibly eye closure.

Future and Controversies

The relative roles of stereotactic radiation and surgery will remain controversial until the
long-term results of radiation treatment protocols are clearly defined.