Introduction
Tinnitus is the phantom perception of sound in the absence of a bona fide sound stimulus
and is not akin to auditory hallucinations (e.g., voices) which are typically associated
with mental illness. Tinnitus (e.g., ringing, buzzing, hissing, etc.), can be perceived
in the head (tinnitus aurium), or in either one (unilateral), or both (bilateral)
ears. Sound perception can be pulsatile (e.g., hearing the heartbeat in the ears),
nonpulsatile, subjective (most common form; only the patient perceives) or is objective
(heard by the examiner, known as somatosound, e.g., turbulent blood flow at the cranial
base, stapedial myoclonus, etc.).
Tinnitus is highly prevalent with an estimated 10 to 15% of the U.S. adults being
affected.[1] Military personnel are particularly at risk and tinnitus is the number one service
related disability, with nearly 750,000 veterans receiving associated compensation
at a cost of over $2 billion in 2014.[1] Hearing impairment, advancing age, noise-exposure, and being male (particularly
in military and combat zones) have been identified as the most relevant risk factors
for tinnitus.[2] Tinnitus is a global problem with many at risk populations. Due to the vast heterogeneity
in symptom presentation and onset, resultant variability in tinnitus perceptions often
leads to considerable gradations in patient frustration, hypersensitivity to sound
(hyperacousis), sleep disruption, and even manifestations of clinical depression and/or
anxiety.[3]
Tinnitus Etiology (Non-Skull Base Tumor Causes)
The underlying etiology of tinnitus is not well-defined, yet has been typically associated
with peripheral ear pathology or disturbances leading to aberrant neural activity
within central auditory and even nonauditory brain stations and pathways.[4] Most tinnitus cases (non-skull base tumor related) result secondary to peripheral
auditory lesions/pathology (e.g., cochlear/auditory nerve) and include, but are not
limited to, sudden sensorineural hearing loss, noise exposure or noiseinduced hearing
loss (most common cause), head or neck trauma, chronic neck or jaw problems, systemic
ototoxic therapies, acute or chronic otologic infection, or iatrogenic (surgery) causes.
Alternatively, damage or compression of the auditory nerve (e.g., microvascular compression
from skull base mass; e.g., vestibular schwannoma) can also lead to tinnitus perception.
Medical/Systemic Causes
Phantom sound perception secondary to hearing loss is a common clinical scenario,
yet this cause and effect relationship is not clearly delineated as many patients
who suffer from debilitating and profound levels of hearing loss do not endorse tinnitus
percepts. Conversely, many who suffer with tinnitus do not show detectable objective
levels of hearing loss per traditional audiometric booth testing.[5] While this observation may not account for the possibility of occult (e.g., hidden
hearing loss) or subtle hearing loss, it highlights and suggests other nonhearing
loss etiologies of tinnitus. Objective forms of tinnitus typically present as pulsations
akin to heart beats appreciated in the ear that are often unrelenting and typically
caused by increased turbulent blood flow within the cranial base vasculature, idiopathic
intracranial hypertension (pseudotumor cerebri), vascular abnormalities (e.g., arteriovenous
malformations), skull base carotid artery bony dehiscence, sigmoid sinus dehiscence
or diverticula, carotid artery dissection, or stenosis. Other identified causes of
objective tinnitus include middle-ear myoclonus (stapedial or tensor tympani), otoacoustic
emissions and superior semicircular canal dehiscence syndrome (SSCD).
Neural Mechanisms of Tinnitus
The neuropathophysiology of tinnitus is not completely understood. A main theory is
that tinnitus perception is the result of peripheral otologic insults that result
in increased gain of function within central auditory circuits.[6]
[7]
[8] This gain increase is thought to occur in both auditory and nonauditory brain centers
that leads to conscious perception of phantom sound. This hypothesis has been reinforced
by observational studies whereby long-standing tinnitus percepts exist following auditory
nerve surgical transection[9] underscoring the critical involvement of central auditory mechanisms in tinnitus
generation. This notion of homoeostatic plasticity in the form of increased central
gain has been validated in animal models and extends from the brainstem cochlear nuclei
through the midbrain and thalamus up to and including the primary auditory cortex
(A1) to compensate for reduced peripheral input.[6] Within A1, decreased peripheral inputs lead to reduced inhibition in de-enervated
areas with subsequent encroachment of nearby intact regions into the void cortical
regions. This concept of A1 tonotopic reorganization may contribute to tinnitus generation.[10] Interestingly, tinnitus-related activity changes/neurophysiologic correlates (increased
neuron spontaneous firing rates and increased neural synchrony) in the central nervous
system (CNS) are not restricted to auditory pathways.[1]
[11] The involvement of nonauditory brain including the insula, cingulate, and thalamus
explain, in part, the potential etiology for conscious auditory perception of phantom
sound. Both auditory and nonauditory neural changes may be modulated by numerous underlying
neurotransmitter-mediated mechanisms that include but are not limited to acetylcholine,
glutamate, gamma-Aminobutyric acid (GABA), serotonin, and glycine.[10]
Somatic Tinnitus
Somatic or somatoform tinnitus is an emerging and alternative cause for tinnitus perception
in the absence of an objectified hearing loss or hidden hearing loss. This stand-alone
etiology is based on growing evidence that strongly demonstrates somatosensory inputs
from jaw musculature, the face and neck that can directly influence central auditory
neural pathways.[2] This is clinically evident in those who suffer from temporomandibular joint (TMJ)
disorders, cervical spine maladies including arthritis, cervical spine joint and intervertebral
disk degeneration, fibromyalgia, and whiplash injuries that have been linked with
tinnitus perception.[12] The specific neural mechanisms include specific trigeminal nerve and cervical inputs
(from C2 level) to the brainstem dorsal cochlear nucleus.[2]
[13] Evidence also suggests that these inputs can influence A1 neurons as well.[14] Consequently, many patients have the on-demand ability to modulate tinnitus pitch
and perception with head and neck maneuvers that include any head movement, jaw thrust,
rubbing of the face, and changes in temperatures applied to the facial skin. These
percepts may also be modulated by stress and emotional factors highlighting the multifactorial
etiology that may be separate from peripheral auditory deprivation and rather a direct
result of altered somatosensory inputs leading to abnormal central auditory activity.[2] When evaluating patients with tinnitus all relevant head and neck, medical, surgical,
auditory, and somatic factors must therefore be considered.
Treatments
Given the multifactorial nature of tinnitus etiology, touted treatments ideally target
the underlying cause, if they are identified. While there is no definitive treatment
or cure for subjective tinnitus, a broad range of therapeutic approaches exists from
typical masking with sound therapy using broadband or white noise or via traditional
amplification with hearing aids,[15] to cochlear implantation,[16] psychological counseling, cognitive behavioral therapy, pharmacologic management
using off-label medications, and various types of brain and cranial nerve stimulation
strategies.[17] The paucity of data regarding the efficacy of many treatment strategies reflects
the multifactorial nature of this disease and often highlights the placebo and idiosyncratic
effect of treatments in this often, desperate patient population and/or reflects inadequate
clinical research data.[18]
Sound Therapy (Hearing Aids and Cochlear Implants)
A traditional and broadly used treatment approach to manage subjective tinnitus is
the use of environmental white noise or directed sound to mask phantom percepts. The
use of relaxation and masking is designed to create an environment that is less disruptive
than the actual tinnitus percept. Traditional amplification with hearing aids provides
broadband sound stimulation that can completely or partially mask phantom sound perception.
These are ideal options for many patients as the bulk of tinnitus sufferers also contend
with sensorineural hearing loss that is amenable to amplification. The limits of amplification
are usually to the higher frequency ranges (typically tinnitus frequency range < 6
kHz)[15] and therefore this treatment option is unable to rehabilitate pan-frequency sensorineural
hearing loss. In those patients with profound sensorineural hearing loss and tinnitus,
traditional amplification often does not provide meaningful benefit or effective tinnitus
suppression. In those instances, cochlear implantation[16] has been utilized to rehabilitate hearing loss and dampen tinnitus perception for
both bilateral and unilateral instances. While effective this treatment strategy is
not ubiquitous and patients should be counseled about realistic expectations about
symptom control.
Tinnitus Retraining Therapy
Tinnitus retraining therapy (TRT) is a therapeutic approach that utilizes a combination
of psychological counseling and focused sound therapy to improve symptom control.
The rationale for TRT is based on the hypothesis that tinnitus etiology is the result
of abnormal, neural activity within and between both auditory and nonauditory brain
pathways.[19] Therefore, TRT attempts to habituate tinnitus symptoms through counseling to reclassify
the percept from an unnatural sound disturbance to neutral stimuli. The benefit of
adding sound therapy to this approach is designed to reduce phantom sound perception
strength. Limited randomized controlled trials with TRT have led to mix the overall
efficacy outcomes leaving providers and patients with limited conclusions.[19] That coupled with the high cost of TRT, have limited its use.
Pharmacology
While a significant number of pharmacologic agents have been tried to treat the symptoms
of tinnitus, no current drug has been approved by the Food and Drug Administration
(FDA). Off-label uses of many medications have been employed including the anesthetic
lidocaine that has been shown to transiently suppress tinnitus perception.[20] This data suggests that neural sodium channels may potentially serve as therapeutic
targets for treatment. However, like many other off-label medications that have been
trialed for tinnitus treatments, transient improvements in phantom sound perception
suggest that multiple mechanisms or targets may contribute to the underlying etiology.
Other drug classes including anxiolytics, antidepressants, and antiseizure medications
have had limited[21] effect on tinnitus perception. However, these medications have been shown to have
potential benefit in managing the psychological and emotional effects of persistent
tinnitus. Other medications including neural pain medications gabapentin and lamotrigine
have shown some evidence of symptom control.[22] Benzodiazepines as a class of medications have also demonstrated some positive benefits
in that they allow patients to tolerate phantom sound perception rather than alleviating
the actual perception itself.[23] Caution should be exercised with all medications, particularly those like the benzodiazepines
as they have potential for dependence, abuse, and the need to taper off when stopping
usage.
Cranial Nerve and Brain Stimulation
Transcranial magnetic stimulation (TMS) of the brain and select cranial nerves is
a therapeutic approach that employs periodic magnetic pulses transmitted through the
scalp to modulate cerebral cortical activity. The rationale behind this touted therapeutic
modality is modulation or a resetting of aberrant central neural circuits in hopes
of abolishing cellular and system pathways that are contributing to tinnitus generation.
TMS has shown some positive results that are unfortunately not sustained for the long-term.[17]
[24] The primary criticisms of these studies include minimal effects sizes, large individual
variability, and a lack of long-term improvement in perception control. Evidence of
tinnitus control using deep-brain stimulation to portions of the subcortical striatum
(caudate nucleus) suggest alternative noncortical neural targets also exist that may
be of clinical benefit.[25] Less invasive approaches are emerging that utilize vagal nerve stimulation with
paired acoustic stimulation or devices that provide stimulation to the trigeminal
nerve with acoustic pairing have shown preliminary evidence of tinnitus control.[26]
[27]
Skull Base Tumor-Associated Tinnitus
Any tumor located in the cerebellopontine angle (CPA) may cause tinnitus due to mass
effect on the vestibulocochlear nerve. Although uncertain, the pathophysiology appears
to be like other more common types of tinnitus in which peripheral hearing loss leads
to central auditory plasticity and resultant phantom sound perception.[28] Other symptoms that commonly accompany CPA lesions largely result from tumor mass
effect on cranial nerves (e.g., hearing loss, generalized and persistent disequilibrium,
facial weakness and numbness), the cerebellum (e.g., ataxia), and on the cerebrum
(e.g., headache and obstructive hydrocephalus).[29] Vestibular schwannomas (also known as acoustic neuromas) are most common, accounting
for 80 to 90% of CPA mass lesions[30]
[31] followed by meningiomas (5–10%), epidermoid tumors (5–9%), and rare lesions (1–5%).
Tinnitus, hearing loss, and disequilibrium are a classic triad of vestibular schwannoma
(VS) clinical presentation; however, the triad only has a specificity of 10% for VS.[32] Different tumors present with varying patterns of symptomatology and radiographic
characteristics can provide helpful clinical and diagnostic cues to the underlying
pathology.
As discussed, if the root cause of tinnitus perception can be identified there is
a higher likelihood of symptom control. Regarding lateral skull base tumors, if the
anatomy, pathology, and existing audiometric parameters are favorable, the goals of
complete tumor removal with concurrent hearing preservation may ameliorate and even
cure phantom sound perception. As such, the ideal conditions may not always be available
and all treatment options including the risks and benefits of each needs to be thoroughly
discussed with each patient. Treatment choices for these lesions typically includes
watchful waiting with serial surveillance imaging and audiometric testing, microsurgical
resection through either a hearing preservation or ablative approach, and/or stereotactic
radiosurgery/therapy. Often, these tumors are either slow growing or do not grow at
all. For this reason, the first step in treatment is often to observe with serial
imaging to establish the natural growth rate of the tumor assuming the tumor is not
causing debilitating symptoms at the time of presentation/diagnosis.
Vestibular Schwannomas
Epidemiology and Clinical Presentation
Over the past decade, the incidence of VS has increased from 1.5/100,000 person-years
in the 1960s to 4.2/100,000 person-years from 2006 to 2016 (Rochester Epidemiology
Project, Mayo Clinic, Rochester, MN).[33] There is no difference in incidence between men and women and incidence increases
with age (median age is 62).[33] The most common symptoms at time of diagnosis are hearing loss (90% all over; 62%
experience gradual loss), tonal tinnitus in the affected ear (59–70%), trigeminal
nerve dysfunction (33–71%), generalized imbalance (20–45%), and aural fullness (16%).[29]
[33] Although not consistent across all studies, some have found tinnitus at presentation
may be a predictor of poorer overall outcomes, with one study finding an increase
of 2.9 (confidence interval [CI]: 1.1–7.6) in the odds ratio (OR) of tumor growth.[34]
[35] As a result, unilateral tinnitus in the absence of a bona fide history or event
should always be evaluated with an inner ear protocol MRI (magnetic resonance imaging)
to rule out inner ear or retrocochlear pathology to include but not be limited to
a vestibular schwannoma.
Treatment
Observation is the most common treatment choice, with 58% of patients and providers
choosing this approach.[33] No baseline parameters have been found to be predictive of growth; however, growth
in the 1st year is predictive of future growth.[28]
[35] One half to two-thirds have not grown at 5-year follow-up.[28]
[35] Based on data for all diagnosed VS in Denmark since 1976, if the tumor had not grown
after 5 years, it did not grow.[36] Of the patients that had American Academy of Otolaryngology (AAO) class A hearing
(good and preserved hearing, pure tone average less than 30 dB and speech discrimination > 70%),
26% had lost it after 1 year, 45% after 5 years, and 54% after 10 years.[36] Male gender and hearing impairment are predictors of preoperative development of
tinnitus in patients with unilateral sporadic VS, whereas complete hearing loss is
a negative predictor for the development of tinnitus.[37] Although there are no guidelines, a common protocol is to repeat MRI imaging at
6 months. If the tumor has grown more than 2 mm and the patient wishes to continue
with observation, repeat MRI imaging in 6 months. If the tumor growth did not meet
the 2 mm threshold then repeat MRI once per year for 5 years.[38]
If the decision is made to proceed with surgery, the three main approaches are the
retrosigmoid (RS), translabyrinthine (TL), and middle cranial fossa (MCF). The factors
influencing the choice in approach include size and extension of the tumor, presence
of preoperative hearing level and expected ability to preserve based on tumor size,
location, patient's age, auditory brainstem response waveform morphology, and preference
of surgeon and patient.[29] There can be no hearing preservation following TL; however, some providers perform
simultaneous cochlear implantation, usually in cases of bilateral VS or VS in the
only serviceable ear. At least one case report, and more recently a small number of
case series, has also demonstrated benefit of doing so in sporadic VS with normal
contralateral hearing, including improvements in sound localization, hearing, and
tinnitus.[39] Postoperative tinnitus is not specifically related to the surgical approach and
should not be used as the sole reason for performing surgery.[40] It should be made clear that given the strong link between hearing loss and tinnitus
perception, patients need to be aware that if they either lose hearing with a hearing
preservation microsurgical approach or if they expectedly lose hearing with an ablative
approach that phantom perception after surgery could be worse than preoperative levels.
Appropriate alternative treatments (previously discussed above) will have to then
be considered.
Since the literature on CPA tumors largely focuses on hearing loss/preservation and
facial nerve dysfunction, more definitive data needs to be collected on outcomes regarding
tinnitus both pre- and posttreatment regardless of modality (observation, surgery,
or radiation). These data should be collected and considered based on the known close
association between hearing loss and tinnitus generation. As one could hypothesize,
greater rates of hearing loss (either directly or indirectly related to CPA tumors)
will lead to greater rates of tinnitus presentation and heightened symptoms severity.
In a systematic review, Ansari et al analyzed postoperative outcomes of the three
different approaches while accounting for tumor size.[41] They concluded that for tumors less than 1.5 cm, the MCF approach led to decreased
levels of hearing loss compared with RS (43.6 vs. 64.3%), with no statistical difference
in facial nerve outcomes between any of the three techniques.[41] For tumors between 1.5 and 3 cm, there was no difference in hearing outcomes between
MCF and RS but facial nerve dysfunction was lower for RS than both TL and MCF (6.1
vs. 15.8% and 17.3%, respectively).[41] Tumors larger than 3 cm, RS resulted in lower facial nerve dysfunction than TL (30.2
vs. 42.5%).[41] When looking at all intracanalicular tumors, there was no difference in hearing
outcomes between MCF and RS but facial nerve dysfunction rates were higher for MCF
(16.7%) than TL or RS (0 and 4%, respectively, no statistical difference).[41]
Stereotactic radiosurgery (SRS) is an alternative to microsurgical removal with similar
outcomes in selected cases. No conclusive difference in tumor control, hearing outcomes,
or complications has been found between single-dose and fractionated SRS.[29]
[42]
[43] In a review that included data from 4,234 patients, Yang et al (2010) found that
compared with patients receiving doses greater than 13-Gy, using fewer than 13-Gy
dose resulted in statistically significant higher hearing preservation rate (60.5
vs. 50.4%) but lower tumor control rate (90 vs. 94%).[44] In a recent study, serviceable hearing was preserved in 72% of patients who received
primary RT and local control in 94.1% after 10 years.[43] In one study, tinnitus disappeared in 20% of those who had it prior to treatment.[43] Other studies have found overall no statistical change in the rate of tinnitus with
either single-dose or fractionated SRS.[42]
[45]
[46]
No randomized trial has been conducted comparing SRS versus surgery. In two prospective
studies (patient decided treatment), Gamma knife radiosurgery (GKRS) was shown to
be superior compared with surgical removal using the RS approach for both preservation
of serviceable hearing and facial nerve outcomes.[47]
[48] It should be noted that hearing preservation rates in both studies (0–5%) were lower
than those reported in other large volume studies (40–80%).[41] A retrospective study specifically documenting tinnitus outcomes found that patients
who underwent TL had an improvement in both the tinnitus handicap inventory (THI)
and visual analogue scale (VAS), while those who underwent GKRS worsened in both categories.[49]
As discussed previously, tinnitus is not an indication for surgical treatment and
results with radiotherapy are inconclusive. When a patient's main complaint is tinnitus,
treatment modalities specifically aimed at tinnitus could be performed as part of
the observation paradigm. As with treatments for other forms of subjective tinnitus
(discussed above), it is important to counsel patients that phantom sound perception
will likely not go away completely but instead there might be a reduction in the loudness
and its negative effects on quality of life. If hearing loss is present on the affected
side, the masking benefits of hearing aids can be explored. Ambient stimulation (e.g.,
sounds of music and nature), personal listening devices that don't occlude hearing
and total masking therapy may be useful for those that don't benefit from hearing
aids. Cochlear implants concurrently placed during surgical removal are also an option.
Education, counseling and cognitive behavioral therapy are additional modalities that
can be useful.
Neurofibromatosis 2
Neurofibromatosis 2 is an autosomal dominant disease of the NF2 gene on chromosome 22 with a prevalence of 1 in 3,300 to 40,000 with no gender or
ethnicity bias.[50] The defect in the gene leads to a tumor predisposition syndrome, with the hallmark
of bilateral VS occurring in 90 to 95% of patients with the condition.[50] In cases with bilateral VS, the surgical removal should be staged with the second
operation taking place at least 3 months after the first one. Early intervention may
be crucial for hearing preservation.[51] Given the inevitability of bilateral tumors, hearing preservation is paramount and
considerations for cochlear implantation or auditory brainstem implants should be
considered. Unfortunately, there is no specific data describing tinnitus rates and
treatment efficacy in the NF2 populations.
Meningiomas
Epidemiology and Clinical Presentation
Although audiovestibular symptoms occur with less frequency with meningiomas in the
CPA compared with VS, for these lesions they remain the most common presenting symptoms.
Hearing loss at presentation occurs in 50 to 80%, tinnitus in 15 to 60%, and generalized
disequilibrium in 30 to 60%.[31]
[32] Symptoms involving other cranial nerves can provide cues that the tumor is not a
VS. At presentation, patients with meningiomas can experience facial pain and numbness
up to 30% of the time and facial dysfunction is seen in 10 to 50%, compared with less
than 5% in those with VS.[29]
[31] Cerebellar signs (i.e., dysdiadokinesia, ataxia) occur in 30 to 90% of patients
at presentation, a rare occurrence in those with VS.[31] The clinician should also be aware that 20% of adolescents presenting with a meningioma
in the CPA have NF2 gene.[3] Specific rates of tinnitus perception with skull base meningioma are not available
and when considering the onset and management of phantom sound perception in these
patients, a similar approach to counseling and treatments employed for VS should also
be performed.
Treatment
Since meningiomas affect hearing less frequently, the standard approach is RS because
it typically offers ideal exposure to the CPA and to these tumors that are typically
located off center from the internal auditory canal. TL approach offers direct access
to CPA and should be performed if there is extensive IAC involvement and hearing preservation
does not seem viable through preoperative auditory compromise, tumor size, or other
patient factors. The MCF approach can be performed to reach the lateral portion of
IAC for hearing preservation but it is not typically indicated if the lesion extends
more than 1 cm into CPA or if there is no evidence of a CSF cap lateral to the tumor
at the cochlea or if radiographic evidence demonstrates that the tumor directly invades
the cochlear canal and modiolar fibers.[31] Most common complications of RS involve damage to cranial nerve (CN) V (8%), VII
(8%), and VIII (12%).[52] Most of these complications occurred in those that had tumor extension into the
jugular foramen. Of those with normal hearing, 8% worsened (deaf) of those with hearing
deficiency, 70% stayed the same or improved.[52]
Recently, SRS has also been used to successfully treat CPA meningiomas smaller than
2.5 cm. Progression free survival was 98 to 99% at 1 year, 96 to 98%% at 3 years,
93 to 95% at 5 years, and 77 to 87% at 10 years.[53]
[54]
[55] Cranial nerve function was improved in 31 to 34%, unchanged in 49 to 58%, and worsened
in 11 to 17%.[54]
[55] The least likely symptoms to improve were hearing loss and tinnitus, with improvement
in 31% of patients at 3-year follow-up.[54]
Epidermoids
Epidemiology and Clinical Presentation
Epidermoids in the cerebellopontine angle arise from displaced ectodermal cells during
early embryological development or from developing neurovasculature later in embryological
development.[31]
[56] The most common presentation of epidermoids is headache (67%).[57] The most common cranial nerve deficit at presentation involve the vestibulocochlear
nerve but these occur in a fewer percentage of patients compared with VS (50–80%).[32] Trigeminal and facial nerve are involved in 30 to 50%.[31]
Treatment
The most common approach to removal of these is the RS approach, although a frontotemporal
craniotomy with a subtemporal approach can also be performed.[31]
[56] The goal of surgery is to decompress the cyst and remove the capsule completely.[31] There has much debate over the aggressiveness with which to treat these typically
nonmalignant tumors. A recent study by Schiefer and Link which reviewed 20 years of
data from their institution concluded that morbidity and mortality is not increased
in total resection versus subtotal resection if the tumor has not expanded significantly
from the CPA. If the tumor has significantly expanded, there were no differences in
rates of recurrence between total and subtotal removal, indicating that in those cases
it would be reasonable not to pursue total resection.[56]
Microvascular Decompression
Microvascular decompression (MVD) for the treatment of tinnitus is very controversial.
The concept is to remove any potential inciting anatomic structure that could be stimulating
the cochlear nerve leading to phantom sound perception. As such, it has been used
for both nontumor (vascular only) and select tumor cases. The literature describes
the concept of neurovascular conflicts (NVCs; e.g.; trigeminal neuralgia; hemifacial
spasms) and when involving the cochleovestibular nerve could lead to tinnitus. A recent
systematic review included 572 patients from 35 studies.[57] They reported that only 28% of patients with tinnitus had complete symptom of relief
with MVD with more than one complication noted in 11% of patients. Interestingly,
patients with both tinnitus and vertigo had a higher chance of success than in those
with tinnitus alone. Due to low rates of success and substantial complications, they
concluded that MVD cannot be included as a standard treatment method for tinnitus
or vertigo. The controversial portion of MVD is such that it has greater efficacy
and success rates in those patients who suffer from combined symptoms. When combined
symptoms occur, it has been suggested that NVC is the underlying etiology and therefore
MVD is therefore warranted. The authors; however, state that a lack of strong evidence
in the included studies, mandate that MVD be utilized with caution.[57] Further studies and validation are required to determine if patients with single
(tinnitus only) or combined symptoms are indeed better candidates for MVD.
