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Acoustic Neuroma

  • Author: Joe Walter Kutz, Jr, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA  more...
 
Updated: May 13, 2016
 

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 sy 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.

See Vertigo: 5 Case-Based Diagnostic Puzzles, a Critical Images slideshow, to help recognize diagnostic clues in vertigo cases.

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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.

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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.

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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.

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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.

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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 average—a 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.

A study by Lee et al of over 100 patients with acoustic neuroma found that tinnitus was the most frequent symptom accompanying hearing loss. It was also determined that approximately 65% of patients had asymmetrical hearing and that an association existed between greater severity of deafness and lower speech discrimination scores.[2]

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.

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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.

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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 25-50% 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 Labbé 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 Labbé. Sudden occlusion of the vein of Labbé 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 Bill’s 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.

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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.

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Contributor Information and Disclosures
Author

Joe Walter Kutz, Jr, MD, FACS Assistant Professor, Associate Residency Director, Neurotology Fellowship Director, Department of Otolaryngology–Head and Neck Surgery, University of Texas Southwestern Medical School

Joe Walter Kutz, Jr, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, Texas Medical Association, Triological Society, American Neurotology Society, Otosclerosis Study Group

Disclosure: Nothing to disclose.

Coauthor(s)

Peter S Roland, MD Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director, Clinical Center for Auditory, Vestibular, and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Chief of Pediatric Otology, Children’s Medical Center of Dallas; President of Medical Staff, Parkland Memorial Hospital; Adjunct Professor of Communicative Disorders, School of Behavioral and Brain Sciences, Chief of Medical Service, Callier Center for Communicative Disorders, University of Texas School of Human Development

Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha, American Auditory Society, The Triological Society, North American Skull Base Society, Society of University Otolaryngologists-Head and Neck Surgeons, American Neurotology Society, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Otological Society

Disclosure: Received honoraria from Alcon Labs for consulting; Received honoraria from Advanced Bionics for board membership; Received honoraria from Cochlear Corp for board membership; Received travel grants from Med El Corp for consulting.

Brandon Isaacson, MD, FACS Associate Professor, Department of Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center

Brandon Isaacson, MD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, North American Skull Base Society, Texas Medical Association, Triological Society, American Neurotology Society

Disclosure: Received consulting fee from Medtronic Midas Rex Insitute for consulting; Received medical advisory board from Advanced Bionics for board membership; Received consulting fee from Stryker for speaking and teaching.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gerard J Gianoli, MD Clinical Associate Professor, Departments of Otolaryngology-Head and Neck Surgery and Pediatrics, Tulane University School of Medicine; President, The Ear and Balance Institute; Board of Directors, Ponchartrain Surgery Center

Gerard J Gianoli, MD is a member of the following medical societies: American Otological Society, Society of University Otolaryngologists-Head and Neck Surgeons, Triological Society, American Neurotology Society, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Vesticon<br/>Received none from Vesticon, Inc. for board membership.

Chief Editor

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;SymbiaAllergySolutions<br/>Received income in an amount equal to or greater than $250 from: Symbia<br/>Received from Allergy Solutions, Inc for board membership; Received honoraria from RxRevu for chief medical editor; Received salary from Medvoy for founder and president; Received consulting fee from Corvectra for senior medical advisor; Received ownership interest from Cerescan for consulting; Received consulting fee from Essiahealth for advisor; Received consulting fee from Carespan for advisor; Received consulting fee from Covidien for consulting.

Acknowledgements

Douglas D Backous, MD Director of Listen for Life Center, Department of Otolaryngology-Head and Neck Surgery, Virginia Mason Medical Center

Douglas D Backous, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Auditory Society, American College of Surgeons, American Laryngological Rhinological and Otological Society, American Medical Association, Association for Research in Otolaryngology, North American Skull Base Society, Society for Neuroscience, and Washington State Medical Association

Disclosure: Nothing to disclose.

References
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  2. Lee SH, Choi SK, Lim YJ, et al. Otologic manifestations of acoustic neuroma. Acta Otolaryngol. 2015 Feb. 135(2):140-6. [Medline].

  3. Telian SA. Management of the small acoustic neuroma: a decision analysis. Am J Otol. 1994 May. 15(3):358-65. [Medline].

  4. Hansen MR, Clark JJ, Gantz BJ, et al. Effects of ErbB2 signaling on the response of vestibular schwannoma cells to gamma-irradiation. Laryngoscope. 2008 Jun. 118(6):1023-30. [Medline].

  5. Boari N, Bailo M, Gagliardi F, et al. Gamma Knife radiosurgery for vestibular schwannoma: clinical results at long-term follow-up in a series of 379 patients. J Neurosurg. 2014 Dec. 121 Suppl:123-42. [Medline].

  6. Powell C, Micallef C, Gonsalves A, Wharram B, Ashley S, Brada M. Fractionated stereotactic radiotherapy in the treatment of vestibular schwannoma (acoustic neuroma): predicting the risk of hydrocephalus. Int J Radiat Oncol Biol Phys. 2011 Jul 15. 80(4):1143-50. [Medline].

  7. Kim YH, Kim DG, Ho Han J, Chung HT, Kim IK, Song SW, et al. Hearing Outcomes After Stereotactic Radiosurgery for Unilateral Intracanalicular Vestibular Schwannomas: Implication of Transient Volume Expansion. Int J Radiat Oncol Biol Phys. 2012 May 12. [Medline].

  8. Bell JR, Anderson-Kim SJ, Low C, Leonetti JP. The Persistence of Tinnitus after Acoustic Neuroma Surgery. Otolaryngol Head Neck Surg. 2016 Apr 19. [Medline].

  9. Alvarez L, Ugarte A, Goiburu M, Urreta Barallobre I, Altuna X. Change in tinnitus after acoustic neuroma removal using a translabyrinthine approach. A Prospective study. Acta Otorrinolaringol Esp. 2016 Apr 8. [Medline].

  10. Rosenberg SI. Natural history of acoustic neuromas. Laryngoscope. 2000 Apr. 110(4):497-508. [Medline].

  11. Brackmann DE, Fisher LM, Hansen M, et al. The effect of famciclovir on delayed facial paralysis after acoustic tumor resection. Laryngoscope. 2008 Sep. 118(9):1617-20. [Medline].

  12. Chopra R, Kondziolka D, Niranjan A, et al. Long-term follow-up of acoustic schwannoma radiosurgery with marginal tumor doses of 12 to 13 Gy. Int J Radiat Oncol Biol Phys. 2007 Jul 1. 68(3):845-51. [Medline].

  13. Combs SE, Thilmann C, Debus J, et al. Long-term outcome of stereotactic radiosurgery (SRS) in patients with acoustic neuromas. Int J Radiat Oncol Biol Phys. 2006 Apr 1. 64(5):1341-7. [Medline].

  14. House JW, Kutz JW Jr. Bone-anchored hearing aids: incidence and management of postoperative complications. Otol Neurotol. 2007 Feb. 28(2):213-7. [Medline].

  15. Isaacson B, Kileny PR, El-Kashlan HK. Prediction of long-term facial nerve outcomes with intraoperative nerve monitoring. Otol Neurotol. 2005 Mar. 26(2):270-3. [Medline].

  16. Isaacson B, Telian SA, El-Kashlan HK. Facial nerve outcomes in middle cranial fossa vs translabyrinthine approaches. Otolaryngol Head Neck Surg. 2005 Dec. 133(6):906-10. [Medline].

  17. Tos M, Stangerup SE, Caye-Thomasen P, et al. What is the real incidence of vestibular schwannoma?. Arch Otolaryngol Head Neck Surg. 2004 Feb. 130(2):216-20. [Medline].

 
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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.
A small acoustic neuroma within the internal auditory canal is easily observed on postgadolinium MRI.
These large bilateral acoustic neuromas are easily observed on MRI. This patient has neurofibromatosis II. Both tumors were eventually removed, leading to anacusis. Facial nerve function remained entirely normal bilaterally.
The nerves of the internal auditory canal as observed in a cadaveric dissection are shown. The posterior wall of the internal auditory canal has been removed. F indicates the facial nerve. S is the superior vestibular nerve. VIII indicates the statoacoustic nerve as it leaves the brain stem, and P indicates the posterior ampullary nerve. The hollow arrow points to the posterior lip of the boney porous acusticus, and the solid arrow indicates the position of the vestibule. C indicates the cochlear aqueduct.
The bone that must be removed for a middle cranial fossa approach is indicated in yellow. The tumor is in orange.
The bone that must be removed for a translabyrinthine approach is indicated in yellow. The tumor is in orange.
The bone that must be removed for a posterior fossa approach is indicated in yellow. The tumor is in orange.
 
 
 
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