I have been watch and wait since 4/06, starting at 1.3cm x .6 x.6 and just received 10/06/2008 MRI at 1.5 x .9 x .9 with minimal growth from 10/07. However, I am constantly concerned that I have been given a warning and if I don't take it I could get facial paralysis and/or balance problems.
I'm sure many of you are in the same scenario.
I found an article that I am attaching, that gave me some more insight into the chance of getting paralysis and vertigo. It is a very detailed analysis and as one example it states that in many cases if the growth of the AN is slow the nerves are able to obsorbe the movement and no damage is done. At least, I now feel that I better understand my chances of not having or not the problems.
Hope this helps.
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 1-2% in the last decade. Postoperative facial paralysis, once the rule, is now an uncommon permanent sequela of acoustic tumor surgery. Attempts at hearing conservation, unimaginable at the beginning of the 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 theatre, development of facial and auditory nerve monitoring techniques, improved anesthesia, and improved perioperative management have all contributed to enhanced outcomes. Most important has been the relentless striving of hundreds of neurosurgeons and otologists.
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. 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.
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). While most acoustic neuromas grow slowly, some grow quite quickly and can double in volume within 6 months to a year.
While 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 outrun 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 to the surface. Destruction of vestibular fibers is slow; consequently, many patients experience little or no dysequilibrium or imbalance. Once the tumor has grown sufficiently large to fill the internal auditory canal, it may continue growth either by eroding bone or by spilling out 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 venous or arterial 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 come in contact with 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 symptomatology 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 generally comes to abut against the lateral surface of the brain stem. Further growth can occur only by compressing or displacing the brain stem toward the contralateral side. A 4.0-cm tumor often extends sufficiently far anteriorly to compress the trigeminal nerve and produce facial hypesthesia. Growth over 4.0 cm generally results in progressive effacement of the vestibular aqueduct and fourth ventricle with eventual development of hydrocephalus.
Clinical
Unilateral hearing loss is overwhelmingly the most common symptom present at the time of diagnosis and is generally the symptom that leads to diagnosis. Consider any unilateral sensorineural hearing loss 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 averageâ€â€a feature deemed typical for retrocochlear lesions. Such marked reductions in speech discrimination scores (often into the teens or twenties) are not invariable, however. A normal speech discrimination score does not rule out an acoustic tumor. A significant number of patients with acoustic tumors have normal or near-normal hearing or 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, acoustic tumor should be considered in anybody with a sudden or fluctuating loss even if hearing returns to normal.
Patients with acoustic neuroma have normal hearing at the time of diagnosis in 3-5% of cases. Surprisingly, patients with medium and large tumors are nearly as likely to have normal hearing as patients with very small tumors. Not surprisingly, the discovery of acoustic neuromas in persons with normal hearing has been increasing as gadolinium-enhanced MRI is becoming more common. 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 dysequilibrium are uncommon presenting symptoms among patients with acoustic tumors. Rotational vertigo (the illusion of movement or falling) is much more common when tumors are small. In Samii's series of 16 patients with intracanalicular tumors, 75% of patients presented with vertigo. This is an atypically high percentage even for small tumors. Dysequilibrium (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 acoustic tumors 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 seamless 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 (about 10% of patients). The motor fibers in the facial nerve can accommodate very substantial stretching as long as it occurs slowly, and they seem much more resistant to injury than sensory fibers. 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. Even though 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.
Facial weakness is sufficiently uncommon (5-10% of patients) that facial weakness associated with a small or medium-size tumor should raise suspicion that it is not an acoustic neuroma. Entertain other diagnoses, such as facial neuroma, meningioma, granuloma, arteriovenous malformation (AVM), or lipoma. Large tumors (>4.0 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.
