A true “cure” for the most common etiologies of tinnitus remains elusive, but most patients are helped by one of several management strategies. Hearing aids or ear-level sound generators, cognitive-behavioral therapy, and programs such as progressive tinnitus management make a real difference for patients, but implantable devices also can improve patients' hearing or reduce their perception of tinnitus.
Ten to 15 percent of adults experience persistent tinnitus, and approximately 20 percent in that group consider it to be a clinically significant problem. The list of causes is long — exposure to loud sounds, infections, hearing loss, cardiovascular or metabolic disorders, neoplasms, head trauma, or medications such as quinine, salicylates, or loop diuretics — but tinnitus usually results from damage to peripheral auditory structures that also results in hearing loss.
In some, peripheral damage causes an imbalance of neural excitation or inhibition that gives rise to the perception of tinnitus. Animal and human studies have demonstrated that tinnitus is associated with abnormal neural activity in central auditory pathways, a finding supported by several functional imaging studies showing that those with tinnitus have increased activity in the auditory cortex, even in the absence of external auditory stimuli. (J Otorhinolaryngol Relat Spec 1996;58:195; Neuroradiology 2007;49:689.) In most cases, if patients' hearing is improved or partially restored, their perception of tinnitus will decrease. (Otolaryngol Head Neck Surg 2006;134:132.)
Tinnitus contributes to depression, insomnia, anxiety, and obsessive-compulsive disorder in some patients, and it is associated with reduced productivity and increased costs for medical care, compensation, and rehabilitation, making management a real imperative.
When sound waves strike the eardrum, tiny vibrations are normally transferred to the middle ear bones, then to the cochlea. In a disease such as otosclerosis, abnormal calcium deposits on the middle ear bones, especially the stapes, and cochlea, impede sound vibrations from being transferred from the eardrum to the inner ear, resulting in progressive hearing loss and sometimes tinnitus. Stapedectomy surgery removes the calcified stapes bone and replaces it with an implanted prosthesis such as a full or partial replica of the stapes, and usually improves patients' hearing and reduces the perception of tinnitus.
Because the cochlea is extremely sensitive to physical vibrations, the force applied during stapedectomy surgery sometimes transfers unnaturally large and harmful vibrations to the inner ear, resulting in permanent hearing loss or tinnitus. Improved surgical techniques such as lasers have reduced the likelihood of this negative outcome.
A study of 19 patients with preoperative severe tinnitus undergoing stapedectomy resulted in 10 patients with complete remission of tinnitus and seven with significant improvement in tinnitus severity. (Adv Otorhinolaryngol 2007;65:343.) Two patients had no change, and none reported worsening of tinnitus after surgery.
BONE-ANCHORED HEARING AID
A titanium prosthesis called an abutment, which resembles the bottom half of a snap on a garment, is surgically implanted into the lower rear region of the patient's skull. After allowing for healing, the bone-anchored hearing aid attaches to the abutment and transmits sound vibrations to the skull and inner ear, bypassing the external auditory canal and middle ear. These hearing aids were designed to help people who have chronic inflammation or infection of the ear canal and cannot wear conventional hearing aids, those with conductive hearing loss or malformed or absent outer ear and ear canals (as occurs in Treacher-Collins syndrome or microtia), and those with unilateral deafness.
Most of the eight patients with significant hearing loss and tinnitus who received bone-anchored hearing aids in another study reported that sound amplified by the aid helped make their tinnitus less noticeable. (Int J Audiol 2002;41:293.) Some patients with more severe tinnitus benefited from a bone-anchored sound stimulator that was custom-made for the study.
MIDDLE EAR IMPLANT
Symphonix developed an implantable middle ear hearing device called the Vibrant Soundbridge in the 1990s. Unlike conventional acoustic hearing aids, this hearing aid bypasses the ear canal and eardrum by directly vibrating the small bones in the middle ear. No portion of the device is placed in the ear canal.
The Vibrant Soundbridge was approved by the FDA for adults with moderate to severe sensoneural hearing loss who wanted an alternative to acoustic hearing aids. The device is now distributed by Med-El in Durham, NC, which also manufacturers cochlear implants.
Dr. Ebherd Biesinger, a hearing researcher in Traunstein, Germany, studied eight patients with hearing loss and severe tinnitus fitted with a Vibrant Soundbridge. When switched on, the device improved hearing and reduced the perception of tinnitus in patients for whom conventional sound stimulation treatments were not helpful.
During the past four decades, more than 200,000 people around the world received cochlear implants, including approximately 43,000 adults and 28,000 children in the United States. Numerous publications have reported that cochlear implantation reduces patients' perception of tinnitus. Yonehara et al reported on 29 cochlear implant candidates, 21 of whom experienced tinnitus before cochlear implantation. (Int Tinnitus J 2006;12:172.) When the implant was activated, seven patients (33%) presented with total tinnitus suppression, and eight (39%) reported partial relief.
Cochlear implantation usually improves hearing and tinnitus on the side of implantation in patients with bilateral deafness, but tinnitus often persists, becomes noticeable, or worsens on the side contralateral to the implant. Bilateral cochlear implantation might be a solution for some patients who suffer these effects.
AUDITORY BRAINSTEM IMPLANT
Auditory brainstem implants were first used in humans in 1979 at the House Ear Institute in Los Angeles. They are approved only for adults and patients with neurofibromatosis type 2 in the United States.
Soussi and Otto found that six of seven patients with neurofibromatosis type 2 who used their auditory brainstem implant daily reported noticeable tinnitus reduction. (Acta Otolaryngol 1994;114:135.) The seventh patient reported no effect. Three other patients used the implant only during laboratory testing, and one reported complete suppression of tinnitus, one described worse tinnitus, and one reported no effect.
More recently, Behr et al reported that auditory brainstem implants improved hearing and reduced the perception of tinnitus for a majority of neurofibromatosis type 2 patients. (Skull Base 2007;17:91.)
For this treatment method, electrodes make contact with neural tissue, and a stimulator unit is implanted beneath the patient's skin, usually below the clavicle. An external device is used to control the stimulator, which delivers electrical current through wires to the electrodes.
Deep brain stimulation involves surgical implantation of long electrodes into the brain to deliver electrical impulses to specific regions. This has provided therapeutic benefits for otherwise treatment-resistant disorders such as chronic pain, Parkinson's disease, tremor, and dystonia.
Shi et al interviewed seven patients who were implanted with deep brain electrodes in the thalamus for movement disorders. (Otolaryngol Head Neck Surg 2009;141:285.) All patients experienced chronic tinnitus, and although the electrodes were not positioned in auditory regions of the brain, three patients reported reduced tinnitus loudness when deep brain stimulation was activated.
Cheung and Larson took a more proactive approach to test the efficacy of deep brain stimulation for tinnitus. (Neuroscience 2010;169:1768.) They enlisted six patients with tinnitus who were scheduled to undergo deep brain stimulation surgery for Parkinson's disease and essential tremor. Although the final target for electrode implantation was the subthalamic nucleus or the ventral intermediate nucleus, the electrode was paused during surgery in the caudate to deliver electrical stimulation there. The lead tip traversed the caudate in five subjects, and tinnitus loudness in both ears was suppressed to a level 2 or lower on a 0-10 rating scale. The tinnitus did not change in one subject where the DBS lead was outside the caudate region.
These reports are encouraging, but it is important to consider the risks and benefits of this invasive procedure for a symptom that is not life-threatening. If deep brain stimulation was preformed for tinnitus specifically, how would a target for stimulation in the brain be selected? Cheung and Larson might argue for the caudate region, but other candidates could be the auditory cortex, the medial geniculate region of the thalamus, the inferior colliculi, or the cochlear nucleus in the brainstem.
BRAIN SURFACE ELECTRODE IMPLANTS
Electrode arrays near the surface of the brain also can be used to stimulate specific neural regions. Subdural electrodes, for example, have been implanted in patients to reduce epileptic seizures or neuropathic pain. De Ridder et al implanted an array of extradural electrodes over the secondary auditory cortex in five patients with chronic tinnitus. (J Otorhinolaryngol Relat Spec 2006;68:48.) The patients were asked to rate their tinnitus distress and loudness on a visual analog scale before and after 40 Hz tonic and 40 Hz burst (five pulses at 500 Hz) stimulation, and they reported significantly better suppression for narrowband noise tinnitus with burst stimulation compared with tonic stimulation. No difference was found between tonic and burst stimulation for pure tone tinnitus.
A study by Friedland et al implanted epidural electrodes over auditory cortex in eight tinnitus patients. (Otol Neurotol 2007;28:1005.) Patients had holes drilled in their skulls, wires were tunneled beneath the skin in their neck, and an electronic stimulation device was implanted beneath the skin below their clavicle. They then spent a night in the neurointensive care unit. Two patients had persistent reduction of pure-tone tinnitus and six patients had short periods of total tinnitus suppression with continuous chronic stimulation. Significant improvements in the Beck Depression Inventory and tinnitus questionnaires were found, although objective measures of tinnitus loudness remained fairly stable.
Neurosurgery carries significant risks so is implantation of brain surface electrodes a viable treatment for tinnitus? Many questions need to be addressed, including which side of the patient's brain should receive the implant? De Ridder et al said unilateral tinnitus is generated by contralateral auditory cortex, and this team surgically implanted stimulating electrodes over this area in attempts to suppress tinnitus. (J Otorhinolaryngol Relat Spec 2006;68:48; J Neurosurg 2004;100:560.) Neural imaging studies by Arnold et al and other researchers, however, demonstrated that the perception of tinnitus is sometimes generated by activity in ipsilateral auditory cortex so it is likely the De Ridder team in some cases implanted electrodes on the incorrect sides of patients' brains. (J Otorhinolaryngol Relat Spec 1996;58:195.)
VAGUS NERVE STIMULATION
The vagus nerve — the tenth cranial nerve — arises from the medulla in the brain, and travels through the neck, chest, and abdomen where it contributes to the innervation of most internal organs. Eighty to 90 percent of the fibers in the vagus nerve are afferent, and convey sensory information about the state of the body's organs to the central nervous system. The vagus nerve supplies motor parasympathetic fibers to all organs except the adrenal glands from the neck down to the second segment of the transverse colon and also controls a few skeletal muscles. Some efferent actions of the vagus include bronchoconstriction in the lungs, reduced heart rate, and increased activity in the gastrointestinal tract.
The U.S. Food and Drug Administration approved the use of vagus nerve stimulation as an adjunctive therapy for partial-onset epilepsy in 1997 and for treatment-resistant depression in 2005. Researchers at Microtransponder in Dallas recently published a study claiming that electrical stimulation of the vagus nerve “completely eliminated the physiological and behavioural correlates of tinnitus in noise-exposed rats.” (Nature 2011;470:101.) This publication and subsequent media reports generated a great deal of interest in vagus nerve stimulation among clinicians, researchers, and tinnitus patients, but we must remember the original experiments were conducted on rats. How can we know if the rats experienced tinnitus at all or what effect vagus nerve stimulation had on their supposed tinnitus?
Engineer et al hypothesized that vagus nerve stimulation eliminated the perception of tinnitus in rats, but they do not know if stimulation directly affects the perception of tinnitus at all. (Nature 2011;470:101.) Because the vagus nerve has such wide-ranging roles and paths of innervation in the body (human and rat), stimulating it will produce a variety of effects. Some of the efferent effects (bronchoconstriction, reduced heart rate, and increased gastrointestinal tract activity) are predictable, and might affect the ways in which patients perceive or react to tinnitus. The afferent effects of vagus nerve stimulation on central nervous system activity are less well known, but could affect patients' mood, disposition, motivation and, indirectly, ways in which they perceive or react to tinnitus.
Although the FDA approved vagus nerve stimulation for treatment-resistant depression, but a randomized controlled trial of 235 patients by Rush et al concluded no definitive evidence of short-term efficacy for the condition. (Biol Psychiatry 2005;58:347.) We should be wary of initial reports that proclaim the efficacy for the method. In light of this finding, we should be wary of initial reports that proclaim the efficacy of vagus nerve stimulation for tinnitus.
Implantable devices can improve or partially restore hearing, improve patients' communication abilities, and contribute to increased socialization and quality of life, reducing anxiety, depression, and tinnitus severity. Some devices that stimulate cranial nerves or specific brain regions have the potential to reduce patients' perception or severity of tinnitus. But one problem is inherent with all implanted electronic devices: they do not last forever. Eventually, the device will stop functioning because of aging components, failing electronics, or encroachment of the patient's tissues or fluids, sometimes meaning device replacement or removal.
Researchers, clinicians, and medical device companies continue to develop and test various types of implants that strive to can improve hearing and reduce the perception of tinnitus, but patients should thoroughly explore noninvasive strategies for tinnitus relief before undergoing surgery, especially for implantation of experimental devices. We all look forward to technological advances, but we should not allow patients' zeal for a quick fix put them at risk for unproven and potentially harmful procedures.
• Read “Reversing pathological neural activity using targeted plasticity” by Engineer et al at http://bit.ly/tXMYiZ.
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