Acoustic neuromas, also known as vestibular schwannomas, are non-malignant tumors of the 8th cranial nerve. Most commonly they arise from the covering cells (Schwann cells) of the inferior vestibular nerve (Komatsuzaki and Tsunoda, 2001; Krais, 2007).
They can also arise within the labyrinth (Neff et al, 2003). They comprise about 6 percent of all intracranial tumors, about 30% of brainstem tumors, and about 85% of tumors in the region of the cerebellopontine angle — another 10% are meningiomas.
Only about 10 tumors are newly diagnosed each year per million persons (Evans et al, 2005), corresponding to between 2000 and 3000 new cases each year in the US. Another way of looking at this is that an average person has a risk of about 1/1000 of developing an acoustic neuroma in their lifetime (Evans et al, 2005). In Denmark, the annual incidence was estimated to be 7.8 patients operated/year (Tos et al, 1992). As technology has improved, more small tumors have been diagnosed, resulting in a similar estimate of about 10 tumors/million/year.
In patients with hearing asymmetry, it is believed that only about 1 in 1000 has acoustic neuroma (source: NIH), although some report prevalence as high as 2.5% (Baker et al. 2003). The higher prevalence does not correspond to our clinical experience in our practice in Chicago, common sense, or the findings of others. Tos et al (1992) observed that in a randomized Danish population of 40-60 year old men, asymmetrical hearing loss occurred in 8%. Simple math would suggest that if 8% of this group has asymmetrical hearing, there would be 80,000 such men among a million persons. Assuming that all tumors resulted in asymmetrical hearing, then the ratio would be 10/80,000 — roughly 1/10,000.
Acoustic neuromas occur largely in adults — they are very uncommon in children. Only 39 cases in children had been reported in the literature as of 2001 (Pothula et al, 2001).
Causes of Acoustic Neuroma
Acoustic neuroma occurs in two forms: a sporadic form and a form associated with an inherited syndrome called neurofibromatosis type II (NF2). About 95 percent of all cases are sporadic.
NF2 is rare; there are only several thousand affected individuals in the entire United States, corresponding to about 1 in 40,000 individuals (see image below). Roughly 5% of patients with acoustic neuroma have type II neurofibromatosis. More information about NF2 can be found at http://ghr.nlm.nih.gov/gene=nf2
There is presently no evidence that radiation from cellular phones causes acoustic neuroma (Muscat et al, 2002).
SIGNS AND SYMPTOMS:
Diagnosis of an acoustic usually requires either a medical doctor with otologic expertise who can integrate together the entire picture, or an MRI with gadolinium. Because acoustic neuromas are very rare, and MRI’s are very expensive, in our opinion — all patients with a substantial risk of having an acoustic should be evaluated by a medical doctor with otologic expertise. In other words, patients with unexplained stable asymmetrical hearing loss should generally all be evaluated by a medical doctor with otologic expertise. The following text describes how this integration process can be done.
While hearing loss is common in acoustic neuroma (i.e. it is sensitive), there are myriads of other causes of hearing loss (i.e. hearing loss is very nonspecific). Roughly 20% of adults have hearing impairment of 25 db or more (Haggard et al, 1981). Because of the high sensitivity but low specificity, routine use of a very expensive diagnostic test such as a gad-MRI of the IAC’s in all persons with asymmetrical hearing is not always justified. In other words, mistakes are possible. While some clinicians “scan” all patients with asymmetrical hearing – -this is a very expensive way to “find” an acoustic.
Hearing loss is the most frequent symptom of acoustic neuroma, occurring in more than 95 percent of patients. About 90 percent present with a one-sided, slowly progressive hearing impairment. An example is shown below.
Clinicians often attempt to estimate the risk of an acoustic neuroma by looking at the pattern of hearing loss. A high-frequency sensorineural pattern is the most common type, occurring in approximately two-thirds of patients. In the remaining third the next most common observation is hearing loss at low frequency (which would be more typical of Meniere’s disease). Even less commonly, some have the “cookie bite” pattern (suggestive of congenital hearing loss or a noise notch).
A sudden hearing loss occurs in about 25 percent of patients with acoustic neuroma. However, because acoustic neuroma is a rare condition, sudden hearing loss attributable to an acoustic tumor occurs in only 1-5 percent of patients with sudden hearing loss as there are many more common causes (Daniels et al, 2000). Even a sudden hearing loss with complete recovery can be caused by an acoustic(Nageris and Popovtzer, 2003).
Cost of diagnosis to society
Asymmetrical hearing is sensitive but extremely nonspecific for acoustic neuroma. The lack of specificity and rarity of acoustic neuromas compared to the myriad of other causes of asymmetrical hearing makes the “cost” of scanning every person with asymmetrical hearing to find an acoustic in 1/1000 persons (or even less) extremely high. The lack of specificity has been commented upon by Margolis and Saly (2008). This conclusion needs to be tempered by other clinical information – -someone with a progressive asymmetrical sensorineural hearing reduction would (in our opinion) be far more likely to have an acoustic than someone with a static or improving asymmetry. Nevertheless, if the chance of finding an acoustic in someone with asymmetrical hearing is between 1/1000 and 1/10,000 and the cost of an MRI is roughly $2000, then it costs between 2 million and 20 million $ in MRI studies to diagnose every acoustic neuroma.
Specificity is another consideration. In this regard, some find that hearing is completely normal in as many as 11% of patients (Morrison and Sterkers, 1996). In our opinion, this percentage is high, but nevertheless certainly acoustic neuroma’s can be found in persons with symmetrical hearing.
Tinnitus is very common in acoustic neuroma, is usually unilateral and confined to the affected ear. Looking at things the other way, if you have tinnitus, it is very very unlikely that you have an acoustic neuroma, because these tumors are far rarer than other mechanisms of ear damage.
In spite of the usual origin of acoustics in the inferior vestibular nerve (Komatsuzaki and Tsunoda, 2001; Krais et al, 2007), vertigo (spinning) prior to surgery is not common, occurring in only about 20 percent of persons with acoustic neuroma. As the inferior vestibular nerve innervates the posterior semicircular canal and saccule, one might expect VEMP’s, which test saccule function, to be uniformly abnormal in acoustic neuroma’s, and in fact they are quite sensitive. Similarly, one might expect ipsilateral BPPV to be rare. This question has not been addressed. One might also expect abnormalities in OAE’s as auditory efferents enter the cochlear area via the inferior division of the nerve. Again, this question has not been addressed.
Vertigo is more common with smaller tumors. Unsteadiness is much more prevalent than vertigo, and approximately 70 percent of patients with large tumors have this symptom. Cerebellar symptoms (i.e. poor coordination of the arms) are unusual.
Hyperventilation induced nystagmus is a little known physical sign that may be far more specific for acoustic neuroma. Evaluation of HVIN requires more sophisticated equipment than is available in most offices. It also requires the examiner to be familiar with this sign — and it is somewhat obscure.
Numbness in the face
Facial sensory disturbances occurs only in large tumors (about 50 percent of those greater than 2 cm in size). The facial sensory disturbance may respond to carbamazepine or oxcarbamazine medication for neuralgia. Facial weakness is uncommon. Facial twitching, also known as facial synkinesis or hemifacial spasm, occurs in about 10 percent of patients. Headache prior to surgery occurs in roughly 40 percent of those with large tumors.
ACOUSTIC NEUROMAS TREATMENT
Nikolopoulos and O’Donoghue recently reviewed 111 articles on acoustic neuroma treatment and stated that “well-designed comparisons between treatment methods do not exist, and therefore claims by clinicians favoring a particular treatment are unfounded” (2002). We do not think that clinical wisdom can be discounted to such a great degree, but certainly the present situation seems to be that acoustic neuroma treatment is an art.
There are three distinct options:
* medical management or “wait and see” (conservative management)
* surgery to remove the tumor
* gamma-knife procedure or stereotactic radiotherapy.
Medical Management: About 25% of all acoustic neuromas are treated with medical management. Medical management consists of periodic monitoring of the patient’s neurological status, use of hearing aids when appropriate, and periodic imaging studies (such as MRI’s). It is an appropriate method of management in some patients (Hoistad et al, 2001).
There is no medication known to have a substantial effect on the growth of acoustic neuroma tumors. The tumors may grow very slowly, about 1 1/2 mm/year, and one may elect to follow a tumor with serial audiometry and/or MRI scans (Shin et al, 2000). In individuals of advanced age, a serious threat to life or bodily function from tumor growth may be judged unlikely in the remainder of a patient’s expected lifespan, and for this reason, medical management may be elected (Perry et al, 2001). Once a tumor is diagnosed, a repeat scan is obtained at 6 months and then at yearly intervals (Perry et al, 2001).
This procedure has its own risks. Even when the tumor is not growing on MRI, there is a risk of losing useful hearing in this situation, making the individual no longer a candidate for hearing preservation type surgery. Somewhere between 10 and 43% of patients followed for about 2 years lose “useful” hearing (Warrick et al, 1999; Shin et al, 2000; Lin et al, 2005).
On the other hand, no matter what treatment procedure is used, surgical or not, in the long term, retention of “serviceable” hearing is very unlikely. The so-called “hearing preservation surgery” rarely preserves useful hearing, and it also tends to deteriorate fairly rapidly with time, with or without a tumor still being there. Because of this observation, some surgeons simply recommend taking out the entire 8th nerve when most convenient as this approach makes tumor recurrence very unlikely. In our opinion, this is should be a judgment call — but not an unreasonable idea. A reasonable estimate is that over a year, about 75% of tumors will have visible enlargement, averaging 1.5 mm, and about 25% will not. Some variants grow much faster than others.
In persons with neurofibromatosis, hearing is likely to remain stable in un operated ears for about 1-2 years (Masuda et al, 2004).
Gamma Knife: When the risk of surgery is high because of other medical problems, or where the patient simply refuses surgery, the “gamma knife” procedure may be used. This is a method of irradiating the tumor, invented by Lars Leksell in 1971. This procedure avoids surgery with its attendant risks. In the past, this option was usually recommended only for higher risk surgical cases because of the possibilities of late radiation complications, and the need for ongoing MRI monitoring of the results of the procedure.
The author of this review does not favor high-dose gamma knife because of the possibility of radiation complications at 2 years and beyond. However, low dose gamma knife is looking much better and there are certainly many times when it is the best option. Lower doses of radiation (e.g. 13 Gy) are presently advised because of the much lower risk of facial weakness and numbness (Wackym et al, 2004).
An interesting consequence of the lower-dose radiation protocol is that patients are now seen who do not have complete loss of hearing or vestibular function after radiation. In some cases this can be very annoying as it may result in nerve irritability symptoms such as hyperventilation induced nystagmus. This is probably a consequence of using a treatment methodology that works more slowly than surgery. It seems likely that this complication is more common in persons who have small tumors.
Hyperventilation induced nystagmus for this situation beats towards the lesion (unlike vibration induced nystagmus which beats away from the lesion). It is often very powerful. In persons with this sign, one can either wait for it to go away (this may take several years), try a medication that reduces nerve irritibility, or reconsider surgical treatment.
Stereotactic radiotherapy. Radiation other than gamma rays can also be used to treat acoustic neuroma. It is similar to gamma knife in it’s overall features. Long term hearing preservation is very rare in persons with Stereotactic radiotherapy (6.7% according to Lin et al, 2005). We see no particular reason to seek out Stereotactic radiotherapy rather than gamma knife. The chance of recurrent tumor using current dose regimens is roughly 5-10%. Tumor growth is rare in patients who remain stable 6-7 years post therapy.
Issues in radiotherapy are recurrence (5-10%), hearing loss, risk of radiating large (>2 cm) tumors due to swelling of the tumor in the first year, risk for malignancy, hydrocephalus, ruptured IAC aneurysm, and accelerated vertebrobasilar atherosclerosis (Jackler, 2007).
Very large acoustic neuroma (coronal view, the tumor is the large white blob). Source: Mayo Clinic Neuroscience Update.
Surgical Treatment: About half of all acoustic neuromas are presently treated with surgery. This option will likely decline over the next few decades as use of gamma-knife treatment grows. The figure above shows a large acoustic neuroma in which surgical management would generally be preferred. In most instances surgical removal of the tumor is the preferred option because it prevents potentially fatal complications of tumor growth (although this would be very unusual). Surgery may theoretically enable “preservation” of hearing, although it is very rare that hearing is actually serviceable after surgery. Usually the surgery is done at an academic center by a team of surgeons including a neurotologist (a specialized otolaryngologist) and a neurosurgeon. There are several operative approaches.
Common surgical approaches to Acoustic Neuroma
- Translabyrinthine (through the inner ear). Hearing loss is expected and inevitable. Not appropriate for very large tumors.
- Retrosigmoid or suboccipital (through the skull behind the ear). Retraction of the cerebellum (part of the brain) is necessary. Headaches are common after this approach.
(Image from Jackler R, Atlas of Neurotology and Skull Base Surgery (Mosby 1996, First edition, with permission).
The translabyrinthine approach makes no attempt to preserve hearing, and does not open the skull. This approach is generally a good one.
See Video: Endoscopic Surgery of Acoustic Neuroma
The middle fossa approach (not shown above), can theoretically preserve hearing, but like the retrosigmoid, the approach is intrinsically more dangerous as it involves retraction of the brain, and also more prone to complications.
Compared to radiosurgery, the primary advantage of conventional surgery is avoidance of late complications associated with radiation affects on neighboring structures. This is a reasonable consideration which, in our opinion, makes conventional surgery advantageous when the patient is a reasonable surgical risk.
Each of these surgical approaches has advantages and disadvantages that must be considered in selecting an optimal approach. Surgical treatment where the brain is exposed is nearly always performed by a team of surgeons, usually including a neuro-otologist and a neurosurgeon. Most patients are admitted to the hospital a day before the operation. After surgery, they spend a night in a monitored unit. Most are discharged from the hospital within 4-6 days after surgery, and return to work is usually possible in 6 weeks. MRI’s are usually obtained at 1 and 5 years to detect residual or recurrent tumor. Total or near total (95%) removal of the tumor is advised (Sanna et al, 2002). Careful follow up with MRI is advised to detect recurrence. Nodular or progressive enhancement in the internal auditory canal may represent regrowth (Brors et al, 2003).
Tumors that extend into the labyrinth itself (i.e. “intracochlear schwannomas”) may not be removed by the “retrolab” approach to tumors, and may recur. There arealso many significant complications that can result from surgery that should be considered (see below).
With respect to hearing preservation surgery, while of course this is certainly desirable, unfortunately the chance of hearing being preserved after acoustic neuroma surgery is slight. Nedzelski and colleagues recently reported that only about 16% of patients had “serviceable” hearing in the follow up interval after “hearing preservation surgery”. (Lin et al, 2005). While hearing may be “preserved” immediately after surgery, it usually deteriorates in most within a few years.
Dr. Hain’s approach.
At the author’s clinical practice in Chicago Illinois, it is suggested that prospective operative candidates primarily consider safety and the probability of complications when considering surgery or gamma knife. If one has serviceable hearing, and there is no other danger of waiting (such as needing a bigger operation), one might reasonably simply wait until hearing becomes unserviceable before proceeding with surgery or radiation. Here the procedure would be periodic hearing tests, and less frequent MRI scans. The frequency of testing is mainly determined by the rate of change in the measures, but about every 6 months for hearing testing and about once/year for MRI scanning is usually appropriate.
Both surgery and gamma-knife methods of managing acoustic tumors seem reasonable at this writing, with the choice depending on individual factors. Surgical management has the advantage that it “gets it over with quickly”. Gamma knife is less acutely stressful, but it can delay resolution of dizziness.
In most instances, acoustic neuroma surgery results in complete loss of vestibular function on the operated side. Gamma knife also is associated with substantial decline in vestibular function (Wackym, 2004). Patients frequently experience vertigo and imbalance post-surgery (Levo et al, 2004; Tufarelli et al, 2007). Vestibular rehabilitation may speed recovery from this deficit. Unless there already is complete loss of vestibular function prior to surgery or radiation (as documented on ENG), we think it is best that the patient who is planning to have acoustic neuroma surgery visit a vestibular physical therapist to make sure that there is a “good fit” and to learn the basic procedures, and for the individual to begin a weekly program of PT for 1-2 months following discharge. It is important that the otologic surgeon who performs the operation be involved with the therapy as in some situations (i.e. patients with CSF leak), therapy should be delayed.
Special Populations and Management
Piazza and others recently suggested that in the elderly, the following algorithm should be followed: If the acoustic protrudes less than 1 cm into the cerebellopontine angle, an MRI should be repeated in one year. If the growth rate is < 2 mm/year, the patient should be observed. If greater than this, offered surgery. According to Piazza, for tumors that protrude > 1 cm into the CP angle, patients in good general health should be offered surgery. Patients in poor general health should be offered radiosurgery (Piazza et al, 2003).
Complications and consequences of acoustic neuroma surgery:
Surgical treatment, per se, has a substantial risk. Overall, the risk of death from acoustic neuroma surgery is about 0.5 to 2 percent. Unexpected post-operative complications occur in roughly 20 percent with more complications occurring in elderly and infirm individuals and those with large tumors (Kaylie et al, 2001). Complications, ordered from rare to frequent, are listed.
* Stroke (rare)
* Injury to cerebellum, pons or temporal lobe (rare)
* Death (about 1/2 percent to 2 %, depending on the center)
* CSF leak (5-15 percent of all patients)
* Meningitis (2-10 percent)
* Facial weakness (4 to 15 percent incidence of total paralysis). Tumor size is a large factor in this complication.
* Hearing loss risk (immediately after surgery)
o Translabyrinthine — 100%
o Retrosigmoid — 60%
o Middle fossa – -40%. Hearing occasionally improves for the middle fossa approach (Stidham and Roberson, 2001).
* Headache (persistent in 10-34 percent, Ruckenstein et al 1996; Soumekh et al, 1996)
* Imbalance and dizziness (almost all patients who have any vestibular function prior to surgery, will have worsening of balance after surgery). This is not a complication, but a consequence.
A recent review of complications of surgery suggested that CSF leak (9.4%) and meningitis (1.5%) are the most common complications (Slattery et al, 2001).
In a review of results of 258 patients operated via the translabyrinthine approach, stroke or cerebellar injury occurred in 1.1%. Cerebellar injury can occur due to traction as well as due to injury to branches of the anterior inferior cerebellar artery (Hegarty et al, 2002). An image of a traction injury is shown below.
There is overall a 0.5 percent incidence of death due to acoustic neuroma surgery. Discharge to long-term care (1.2%), to short-term rehabilitation (4.4%) are also possibilities (Barker et al, 2003). Thus, there is roughly a 1.7% chance of death or long term nursing care being required after acoustic neuroma surgery. The odds are better if one chooses a “high volume” hospital and surgeon.
Other complications include CSF leak in 7.8%, meningitis in 1.6%.
Facial weakness of various degrees appeared in most, but severe weakness with House-Brackman scores of V-VI at 1 year occurred in 6% (Mass et al, 1998). Wiet and others have recently reported results in 500 cases (Wiet et al, 2001). Overall success at retaining useful hearing was 27%, with considerably better results obtained when operating via the middle-fossa approach.
Hearing “sparing” surgery is usually just wishful thinking.
Hearing in the operated ear often deteriorates over time to a greater extent than the unoperated ear, even without recurrent tumor (Chee et al. 2003). The percent of persons with “serviceable hearing” may deteriorate by 25% in the late post-operative period. This has been variously attributed to scarring, fibrosis, or microhemmorages during operation. Over the long term, very few patients retain serviceable hearing (Lin et al, 2005). Some authors have suggested that given the modest hearing that is salvaged in the very few patients who are candidates for hearing sparing surgery, that hearing preservation as an objective of acoustic neuroma surgery is not worthwhile (Tos et al, 1988). Our view is that it is occasionally worth attempting, but one’s expectations should be realistic.
Balance is usually worse after acoustic neuroma surgery
This is simple stuff — balance deteriorates after acoustic surgery because the surgery damages or removes remaining function in the vestibular nerve (Levo et al, 2004; Tufarelli et al, 2007). Tufarelli and associated reported that 10% of 459 patients judged their imbalance as disabling, and 73% felt that they had at least moderate oscillopsia (trouble seeing with head moving).
MRI scan from person who had acoustic neuroma removed via retrolab approach, and with refractory dizziness. On the right side of the picture (left side of head), there is a black area where there was damage to the cerebellum, presumably associated with the surgery.
It has been our experience that over the long term (i.e. 2 years), balance generally returns to near normal, but persons who have other deficits such as visual disturbances (e.g. cataract), sensory loss (e.g. neuropathy), brain damage (e.g. cerebellar or brainstem damage due to the tumor or surgery), or poor adaptation (e.g. due to advanced age) may never obtain complete return of balance.
Another scan showing cerebellar damage following acoustic neuroma surgery. This type of injury will most likely be accompanied by permanant imbalance due to the combination of a cerebellar injury and loss of inner ear function on the left.
At a recent meeting at the ANA (acoustic neuroma association), the author of this page participated in a 2-hour session and interviewed 8 patients who had persistent vertigo. As a general rule, patients who had vertigo 2 years following surgery, had had a mixture of a cerebellar injury and total vestibular loss, associated with a difficult surgery (usually for a 4cm + tumor). The MRI scan of two patients are shown below. As a general rule, patients who have lost both inner ear function (from the acoustic), and substantial cerebellar function (from the surgery or acoustic), will have an enduring loss of balance.
Tumor operated in 1961. There is clear cerebellar damage on the left side of the cerebellum (right side of picture).
Immediately after surgery, most patients have vertigo.The timing and prognosis of this vertigo depends on the reason and associated damage to the cerebellum (if any). A detailed discussion of dizziness, vertigo and imbalance, pre and post surgery can be found in this lecture handout.
Significant headache can occur following acoustic neuroma surgery (reviewed by Driscoll and Beatty, 1997). The incidence is very variable among surgeons and also depends on the choice of approach, but an overview of the literature suggests an incidence of about 20-35%. This compares with an incidence of about 8% after radiosurgery.
Schessel et al (1996) observed and documented adherence of neck muscles to the dura after craniotomy and reported a dramatic decrease in headache in patients who had craniotomy with replacement of the bone flap. Similarly, Harner also noted a drop in headache when cranioplasty with methyl methacrylate was used instead of craniotomy alone (Harner et al, 1995). The mechanism here is thought to be traction on the dura by movement of neck muscles. Many patients with this syndrome note aggravation by coughing or straining.
Schessel et al (1996) suggested that patients having surgery via the retrosigmoid approach had significantly higher frequency of headache than those who had the translabyrinthine approach. Several other groups have found a similar pattern. Schaller and Bauman (2003) noted severe headaches requiring daily medication and accompanied by a feeling of incapacity in 34% of patients at 3 months following retrosigmoid surgery. They found that these headaches were associated with aseptic meningitis and furthermore that they were associated with use of fibrin glue and drilling in the posterior aspect of the internal auditory canal. They suggested that prevention of postoperative headache may be accomplished by replacement of bone flap at the end of surgery, use of duraplastic instead of direct dural closure, and avoidance of the use of fibrin glue or extensive drilling of the posterior aspect of internal auditory canal.
Currently there is little information about incidence of headache using the middle fossa approach, but the few series available suggest a rather low incidence (Driscoll et al, 1997).
Management of post-operative headache utilizes analgesics, muscle relaxants, antidepressants and anticonvulsants, in a way similar to migraine management. Migraine abortive agents, however, and specific prophylactic drugs for migraine are not recommended in most instances. Nevertheless, a recent report found that sumatriptan (a migraine drug) improved headache in 9/10 patients with post-surgical headaches. This probably reflects the fact that migraine is an extremely common health condition that worsens with any type of head pain.
Persistent incisional pain may occur from entrapment of the occipital nerve or from formation of an occipital neuroma. Massage, local heat, and analgesics may help. Occipital nerve blocks (such as is done in the pain clinic) may also be beneficial.
Another mechanism that have been suggested is that bone dust trapped within the intracranial cavity may cause a protracted inflammatory response resulting in chronic headache (Driscoll, 1997). MRI images sometimes show dural enhancement (the membrane covering the brain “lights up”) and CT images may show calcification along the brainstem (Schaller and Bauman, 2003). This sort of headache should not respond to blocking of scalp nerves (as is done in the pain clinic) and this procedure may be of some diagnostic use. In these patients, logically treatment might include anti-inflammatory agents and possibly corticosteroids. Narcotic analgesics are occasionally indicated.
Post-operative MRI scans
No standards exist regarding patient follow-up following complete acoustic neuroma resection. On average though, 3 to 6 scans is common over a follow-up period of about 5 years. (Lee and Isaacson, 2005).
Very rarely, a person with an acoustic neuroma might desire a cochlear implant. This might occur if an acoustic tumor is present in the only hearing ear or after surgery to remove bilateral acoustic neuromas. Belal (2001) reported that cochlear implantation is possible only if there is an intact cochlear nerve (as shown by a positive response to promontory stimulation), and if the implantation is done at the time of acoustic tumor removal, before the cochlea ossifies.
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* Presentation by Dr. Hain at ANA association meeting 2009 on balance issues pre and post surgery
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