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Acoustic Neuromas: Symptoms and Diagnosis
Louis J. Kim, MD
Jeffrey D. Klopfenstein, MD
Randall W. Porter, MD
Mark J. Syms, MD*
Division of Neurological Surgery and *Section
of Neurotology, Barrow Neurological Institute, St. Joseph's
Hospital and Medical Center, Phoenix, Arizona
Acoustic neuromas are the most common
cerebellopontine angle tumor in adults. While their natural history
is not fully understood, a subset of tumors demonstrates
significant growth over time, necessitating treatment. Clinical
manifestations include hearing loss, tinnitus, vertigo,
dysequilibrium, and cranial nerve neuropathies. Late findings
include brainstem compression, hydrocephalus, and facial paresis.
Audiometric testing is useful for diagnostic screening and
pretreatment planning. Magnetic resonance imaging is the diagnostic
gold standard. Its widespread use has led to increasingly earlier
diagnosis of acoustic neuromas, including asymptomatic lesions.
Key
Words: acoustic neuroma, audiometry, radiological imaging,
sensorineural hearing loss
A thorough understanding of the clinical manifestations of acoustic
neuromas is essential for diagnosis. Once this lesion is suspected,
the appropriate diagnostic tests are vital for treatment planning
and pretreatment discussions with the patient. This article reviews
the clinical presentation and diagnostic evaluation of acoustic
neuromas.
Epidemiology
Acoustic neuromas account for about 75% of
tumors discovered in the cerebellopontine angle (CPA). Their
prevalence and incidence remain unclear.[15] Schuknecht analyzed
1400 temporal bone specimens and found a 0.57% incidence of occult
acoustic neuromas, or about 570 tumors per 100,000 people.[28] In
another temporal bone study, Leonard and Talbot20 found a 0.8%
incidence of occult acoustic neuromas. However, the 1991 National
Institutes of Health Consensus Statement estimated 2,000 to 3,000
new, clinically apparent cases of unilateral acoustic neuromas each
year,[1] or an incidence of about one tumor per 100,000 per
year.
Given the disparate data between occult
postmortem lesions and clinically apparent lesions, the true
incidence of acoustic neuromas is thought to range between these
two numbers. A large number of clinically silent tumors probably
never require medical attention during an individual's lifetime.
With the widespread use of magnetic resonance (MR) imaging,
however, the diagnosis of clinically occult lesions will increase.
The approach to these diagnosed but clinically silent lesions will
rely heavily on our understanding of the natural history of these
tumors.
Natural
History
Deen et al.[7] followed 68 elderly patients
(mean age, 67.1 years) with acoustic neuromas conservatively for a
mean of 3.4 years; 71% demonstrated no tumoral growth. Eventually
15% required treatment. Glasscock and coworkers[13] followed 34
patients for a mean of 2.4 years. The mean growth rate of 56% of
the tumors was 2.9 mm/year. Mirz et al.[21] reported 50 patients.
The mean growth rate of 64% of the tumors was 1.6 mm/ year. During
a mean follow-up of 4.8 years in 80 patients with no prior
treatment, 42% exhibited no growth.[26] The overall growth rate in
these nonsurgical patients was 0.91 mm/year. Among 49 patient who
underwent subtotal surgical resection, 68.5% exhibited no new
growth.[26] The overall growth rate in this group was 0.35 mm/year.
Three patients (6.1%) subsequently required reoperation due to
regrowth. Yamakami et al.[33] reported 903 patients followed a mean
of 3.1 years: 51% exhibited an average growth rate of 1.87 mm in
the first year, and 20% subsequently required surgical
intervention.
A cadre of small, retrospective, natural
history studies has been reported, but long-term prospective data
are lacking. Therefore, the exact natural history of acoustic
neuromas remains uncertain. A subset of tumors appears subject to
rapid growth while another subset exhibits no growth over time.
Based on current studies, however, it is reasonable to use
serial imaging studies for small tumors, particularly in patients
over 65 years. If rapid growth, new symptoms, or both are
identified, intervention can be instituted.
Clinical
Manifestations
In 1917 Harvey Cushing reviewed his acoustic
neuroma series and extrapolated a progression of neurological
symptoms orresponding to tumor enlargement: gradual auditory and
labyrinthine dysfunction, occipitofrontal pain, cerebellar ataxia,
adjacent cranial nerve palsies, increased intracranial pressure,
dysphagia, dysarthria, and brainstem compression with respiratory
compromise.[6]
Jackler and Pitts[17] used three stages to
describe acoustic neuroma growth in anatomical terms. The
canalicular stage, characterized by hearing loss, tinnitus, and
vertigo, occurs during early growth of the tumor from the lateral
fundus of the internal acoustic canal to the porus acusticus. Early
displacement of cranial nerves against the bony wall of the canal
occurs. During the cisternal stage, auditory and vestibular
function progressively declines and headache occurs from dural
irritation. The tumor grows from the porus acusticus into the 1- to
2-cm subarachnoid cistern adjacent to the brainstem. The facial and
vestibulocochlear nerves and anterior inferior cerebellar artery
are displaced progressively. Progressive nerve dysfunction results
when tumor growth in the CPA exceeds that of the portion in the
internal auditory canal and the facial nerve is stretched over the
bony anterior lip of the porus. Late in this stage as the
trigeminal nerve becomes distorted, midfacial and corneal
anesthesia can manifest. The brainstem compressive stage is
demarcated by tumor growth extensive enough to displace brainstem
structures, to obstruct the fourth ventricle, to deform the
trigeminal nerve and tentorium superiorly, and to deform the nerves
of the jugular foramen inferiorly. At this stage, facial twitch and
weakness, worsening headache, papilledema, and diplopia related to
obstructive hydrocephalus may occur.
Selesnick et al.[30] correlated symptoms with
duration of their onset before diagnosis. Tinnitus and hearing loss
occurred 4 years before diagnosis, vertigo 3.6 years earlier,
headache 2.2 years earlier, dysequilibrium 1.7 years earlier,
trigeminal symptoms 0.9 years earlier, and facial nerve symptoms
0.6 years earlier. The stages of acoustic neuroma growth also were
correlated with symptoms. The canalicular stage occurred 4 years
before diagnosis, the cisternal stage 1.5 years later, and the
brainstem compressive stage 0.9 years later. The authors stress the
importance of the 1.5-year gap between the canalicular and
cisternal stages, during which earlier diagnosis might permit
treatment of a considerably smaller and less symptomatic tumor.
Hearing
Loss
Progressive, high-frequency unilateral or
asymmetric sensorineural hearing loss, the most common symptom of
acoustic neuromas, is reported to occur in more than 95% of
patients.[15,29] It usually develops over months to years and
is associated with impairment of speech disproportionate to the
pure tone loss. In 10% of cases, sudden hearing loss occurs and is
attributable to the vascular interruption of the internal auditory
artery.[5,17] Based on audiometry, speech discrimination
scores, and speech reception thresholds, normal hearing has been
observed in 3 to 15% of acoustic neuroma cases.[4,25] In
these patients, dysequilibrium was the most common
symptom.[27] The mechanism for hearing loss is unclear, but
it appears to be related to the compressive effects of tumor on the
vestibulocochlear nerve with resultant injury to neuronal elements,
vascular compromise, or both.
The Gardner-Robertson hearing classification
system was established to standardize the measurement of
preoperative and postoperative hearing (Table 1).[12] Hearing is
assessed using speech reception thresholds and speech
discrimination scores. In this 5-point grading scale, useful
hearing is scored as I or II, nonuseful hearing (absent speech
discrimination) as III or IV, and complete hearing loss as V.
The Gardner-Robertson hearing classification
system was established to standardize the measurement of
preoperative and postoperative hearing (Table 1).[12] Hearing is
assessed using speech reception thresholds and speech
discrimination scores. In this 5-point grading scale, useful
hearing is scored as I or II, nonuseful hearing (absent speech
discrimination) as III or IV, and complete hearing loss as V.
The Committee on Hearing and Equilibrium of
the American Academy of Otolaryngology-Head and Neck Surgery has
also provided guidelines for reporting pre- and postoperative
hearing function (Table 2). According to these recommendations,
hearing thresholds are reported as the average of puretone hearing
thresholds by air conduction at 0.5, 1, 2 and 3 kHz. In addition,
speech discrimination at levels of 40 dB or maximum comfortable
loudness should be documented pre- and postoperatively. [2]
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Tinnitus
According to Hardy et al.,[15] tinnitus is
associated with 71% of acoustic neuromas at presentation. Unlike
hearing loss, tinnitus has a low impact on patient functioning;
therefore, it rarely serves as the impetus to seek medical
attention. Nonetheless, unilateral tinnitus without obvious cause
warrants investigation of the auditory brainstem response (ABR) or
MR imaging. Tinnitus in the absence of hearing loss is extremely
rare.[10] The pathophysiology of tinnitus associated with acoustic
neuromas is thought to be similar to that of hearing loss, that is,
neural or vascular compression.
Vertigo
Vertigo, the illusion of motion, has been
reported in 58% of patients.[24] According to a University of
California—San Francisco (UCSF) series, vertigo occurred in
19% of patients overall but was inversely proportional to the size
of the tumor. Vertigo was present in 27% of patients with tumors
less than 1 cm compared to 19% of patient with tumors 1 to 3 cm and
10% of patients with tumors larger than 3 cm. Dysequilibrium, the
sense of floating or unsteadiness, was more common (48%
overall),[29] and its incidence was proportional to the size of the
tumor.
Given that acoustic neuromas arise from the
vestibular nerves, it is paradoxical that vertigo is not a more
consistent finding. The pathophysiology of vertigo is believed to
be related to the compressive effects of the tumor on the
vestibular nerve or vascular supply. Because nerve attenuation
usually is gradual, the loss of function is readily compensated for
by the contralateral vestibular system. Thus, symptoms of vertigo
are usually mild unless a large tumor also affects cerebellar
functioning.
Cerebellar
Dysfunction
Cerebellar symptoms, including incoordination,
ataxia, and dysequilibrium, usually occur late in the course of
tumor growth. Symptoms tend to be continuous and unremitting.
Incoordination typically is worse in the lower extremities than in
the upper extremities. Cerebellar involvement tends to include the
flocculus, which is a component of the vestibulo-ocular reflex.
Disruption of the flocculus by tumor compression can lead to
dysequilibrium, truncal ataxia, and nystagmus. Volitional limb
movement remains normal when only the flocculus is involved.
However, if the lesion grows large enough to affect the cerebellar
hemispheres, severe lateral compression can result in ipsilateral
ataxic limb movements, intention tremor, and, in extreme
situations, hypotonia. Trigeminal Nerve Involvement Typical
trigeminal nerve dysfunction related to acoustic neuromas includes
hypesthesia or paresthesias of the midfacial region. Although the
incidence of trigeminal symptoms ranges from 33% to 71%,[29]
several studies have reported a strong correlation between tumor
size and trigeminal symptoms.[22,29,32]
The classic description of early trigeminal
involvement with an acoustic neuroma is loss of the corneal reflex.
Increasing nerve dysfunction related to tumor growth can produce
midfacial tingling that can progress to
numbness.
In extremely large tumors, the muscles of mastication can atrophy.
According to Jannetta,18 10% of trigeminal neuralgia cases are
related to neoplasms, a proportion of which includes acoustic
neuromas. In giant tumors, contralateral tic douloureux can serve
as a false localizing sign. Symptoms arise due to direct nerve
compression in the superior CPA
just inferior to the tentorium.
Headaches
Cephalgia is related to compression and local
irritation of the neural, vascular, and dural contents of the
internal auditory canal or petrous bony dura. Incidence is also
related to tumor size. In the UCSF study, no tumors smaller than 1
cm caused headaches. In contrast, headaches occurred in 20% of
those with 1- to 3-cm tumors and in 43% of those with tumors larger
than 3 cm.[29]
Hydrocephalus
Symptoms from hydrocephalus related to tumor
obstruction of the fourth ventricle include headache, nausea,
vomiting, diplopia, papilledema, and changes in mental status. Its
incidence is low, occurring in 4% of cases according to the UCSF
series.[29] Significant tumor growth is usually required to produce
obstructive hydrocephalus.
Facial Nerve
Involvement
Facial nerve dysfunction occurs late in the
course of tumor growth, and frank facial nerve palsy is usually
preceded by facial twitch and paresis. The facial nerve can
tolerate gradual tumor growth surprisingly well, despite being
splayed and thinned over the surface of the tumor. This effect is
especially likely to occur just medial to the porus acusticus, the
anterior bony lip of which can compress the distorted nerve as it
enters the internal auditory canal. Neural
compression
causing facial nerve dysfunction typically requires a large tumor
mass. Therefore, small CPA tumors associated with facial nerve
dysfunction should signal clinicians to suspect another pathology
such as a facial nerve schwannoma or cavernous malformation
involving the internal auditory canal. The incidence of facial
nerve dysfunction
associated with acoustic neuromas is about 10%.
The sensory fibers of the facial nerve are
often affected, but patients seldom notice a clinical effect.
Hitselberger's sign, hypesthesia of the posterior external auditory
canal and concha skin, can be detected with careful examination.[2]
Lower Cranial Nerve and Brainstem
Findings
Glossopharyngeal and vagus nerve compression
from tumor can cause hoarseness, dysphagia, and aspiration.
Hypoglossal nerve compression can lead to dysarthria. These
findings are always late in the course of an acoustic neuroma
because the tumor must be very large to extend caudally toward the
jugular foramen and hypoglossal canal. Contralateral weakness is
typically a long tract sign related to brain stem compression or
cerebellar tonsillar herniation through the foramen magnum.
However, ipsilateral weakness can also occur.
Diagnosis
Audiologic testing is useful not only for the
diagnosis of acoustic neuromas but also for pretreatment planning
based on the extent of useful hearing. Both pure tone audiometry
and speech audiometry are the first-line tests. Puretone
sensorineural hearing loss is reflected in the shape of the
audiogram: flat, high-tone loss, low-tone loss, and trough-shaped
loss. Johnson found that 66% of patients experienced high-tone
loss, while the other types each occurred in 10%.[19] Analysis of
speech discrimination scores showed that only 28% of patients
exhibited speech discrimination better than 62%. The ability of
audiometric testing to identify all patients with an acoustic
neuroma is imperfect.[29] Therefore, test results should be
interpreted cautiously. Persistent clinical suspicion of an
acoustic neuroma despite normal audiologic tests warrants the
patient undergoing gadolinium-enhanced MR imaging.
Acoustic reflex testing, which monitors middle
ear impedance as an indirect measure of the contraction of middle
ear muscles in response to a loud sound, is independent of the
patient, which avoids biased test results. Acoustic reflex decay is
defined as 50% decay of a tone administered 10 dB above
threshold.[29] The sensitivity of the combined use of acoustic
reflex and decay for detecting acoustic neuromas is as high as 97%.
Low specificity, however, precludes these tests from having an
accurate predictive value for acoustic neuromas.
The most useful and accurate audiologic test
for acoustic neuromas remains the ABR. The prerequisite for this
test is hearing function sufficient to generate an adequate ABR.
The test uses computer averaging over time to filter background
noise to generate an electroencephalogram created by the response
of the auditory pathway to an auditory stimulus. The waveform
represents specific anatomical points along the auditory neural
pathway: the cochlear nerve and nuclei (waves I and II), superior
olivary nucleus (wave III), lateral lemniscus (wave IV), and
inferior colliculi (wave V).
For clinical use, the most reliable waves
generated are the synchronous discharges of wave I from the
cochlear nerve and of wave V from the inferior colliculus. Waveform
characteristics used to detect abnormalities include amplitude,
latency, and the interval difference between the two sides. The
most reliable indicator for acoustic neuromas from the ABR is the
interaural latency differences in wave V: The latency in the
abnormal ear is prolonged (Fig. 1).
Figure 1. (A) Waves I through V of the auditory brainstem response
(ABR). (B) Abnormal ABR during resection of an acoustic neuroma
shows
wave V, an increase in the interaural latency, and a decrease in
amplitude beginning at 13:38. Retraction on the tumor was altered,
and the
ABR returned to baseline by 14:00. The latencies from the affected
left ear and normal right ear are shown for comparison. The traces
move
through time from top to bottom. From Zubay G, Porter RW:
Preoperative assessment of patients with acoustic neuromas.
Operative
Techniques in Neurosurgery 4(1):11-18, 2001. With permission from
Elsevier.
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The advantages of ABR include its relative
imperviousness to general anesthesia and the patient's level of
consciousness. However, the ABR varies with temperature, head
circumference, and menstrual cycle.[8] Several reports have
documented the specificity of ABR for the diagnosis of acoustic
neuroma to be as high as 98% with a specificity of
90%.[11,16,22,23,25] The rate of falsenegative ABRs has been
reported as 2% for acoustic neuromas and as high as 25% for other
CPA tumors.[31]
Stacked derived-band ABR may identify small,
intracanalicular acoustic neuromas with greater sensitivity than a
standard ABR.[9] This technique uses derived-band ABRs obtained up
to normal hearing levels. The stacked ABR uses the amplitude of
wave V as the measurement point: Wave V of each derived-band ABR is
temporarily aligned and the time-shifted responses are summed.
Rarely, a patient with an acoustic neuroma has
normal pure-tone hearing, acoustic reflexes, and ABRs. Thus, any
patient under a high index of clinical suspicion for an acoustic
neuroma should undergo MR imaging.
Imaging
Studies
Gadolinium-enhanced MR imaging offers
excellent resolution of soft tissues, the tumor's size and
morphology, and the relationship between normal and abnormal
anatomy. It is the imaging study of choice to rule out an acoustic
neuroma. Tumor enhancement is usually homogenous. Areas of cystic
structure, necrosis, and hemorrhage can be present in larger
masses.
Acoustic neuromas are usually lobular,
well-circumscribed, and centered over the porus acusticus. They may
or may not demonstrate tumor enhancement into the internal auditory
canal. Larger tumors maintain their lobular shape, leading to
deformation of the adjacent cranial nerves, brainstem, and
cerebellum (Fig. 2).
Figure 2. Contrast-enhanced magnetic
resonance image shows a giant acoustic
neuroma significantly distorting the brain
stem and fourth ventricle. Both enhancing
and cystic components are present.
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Acoustic neuromas are differentiated from CPA meningiomas, the
second most common mass in this region in adults, by the absence of
a dural tail. The latter typically represents enhancement where a
meningioma attaches to its dural base. Dural-based meningiomas also
lack a flattened, broad base along the petrous face (Fig. 3).[3]
Both tumors can extend into the internal auditory canal. The
differential diagnoses for CPA masses also include epidermoids,
choroid plexus papillomas, metastases, arachnoid cysts, schwannomas
involving other cranial nerves, neurenteric cysts, cavernous
malformations, cholesterol granulomas, aneurysms, and
dolichoectatic vertebrobasilar arteries.
Figure 3. (A) Axial magnetic resonance image shows a broad, flat
base along the petrous
bone and dural tail along the anteromedial border (arrow). Both
findings are consistent
with a meningioma, not an acoustic neuroma. (B) The tumor’s
extension into the internal
auditory canal is nonspecific for acoustic neuromas and
meningiomas.
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Computed tomography (CT) is a common screening
tool to rule out mass lesions of the brain. Acoustic neuromas
appear iso- to hypodense on nonenhanced CT and enhance homogenously
after contrast injection. However, CT is inferior to MR imaging in
its resolution of soft tissue anatomy and is subject to
beam-hardening artifact in the bony confines of the posterior
fossa. The latter point has become less troublesome with the advent
of multislice spiral CT scanners.
Nonetheless, CT retains its usefulness in
pretreatment planning because it offers superior imaging of bony
anatomy. Bone windows on CT can show enlargement of the internal
auditory canal related to tumor growth and can exquisitely detail
the relationship of the tumor to the mastoid air cells, transverse
sigmoid junction, jugular bulb, internal auditory canal, and bony
labyrinth.[14] Understanding these relationships facilitates
surgical planning.
Conclusions
Acoustic neuromas are the most common CPA
tumors in adults. Although their natural history is still not
clearly defined, a subset can demonstrate significant growth over
time. The stages of acoustic neuroma growth are well correlated
with symptom development. Depending on their size, acoustic
neuromas typically present with unilateral sensorineural hearing
loss and various degrees of cranial nerve symptoms and cerebellar
symptoms. Audiometric testing can provide useful diagnostic and
pretreatment planning information. Even if audiometric tests are
negative, imaging studies should be obtained if clinical suspicion
remains. Because of its excellent resolution of soft tissue, MRI is
the definitive diagnostic tool. For preoperative planning, CT
provides superior bony detail in relation to the tumor.
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