there were no medications effective for tinnitus. There is not enough evidence to determine if antidepressants or acamprosate are useful. While there is tentative evidence for benzodiazepines, it is insufficient to support usage. Anticonvulsants have not been found to be useful. Steroid injections into the middle ear also do not seem to be effective.

Botulinum toxin injection has been tried with some success in some of the rare cases of objective tinnitus from a palatal tremor.

The use of sound therapy by either hearing aids or tinnitus maskers helps the brain ignore the specific tinnitus frequency. Although these methods are poorly supported by evidence, there are no negative effects. There is some tentative evidence supporting tinnitus retraining therapy. There is little evidence supporting the use of transcranial magnetic stimulation. It is thus not recommended.

Definitive treatment depends on the underlying cause of vertigo. Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet and intratympanic injections of the antibiotic gentamicin or surgical measures such as a shunt or ablation of the labyrinth in refractory cases.

Common drug treatment options for vertigo may include the following:

- Anticholinergics such as hyoscine hydrobromide (scopolamine)

- Anticonvulsants such as topiramate or valproic acid for vestibular migraines

- Antihistamines such as betahistine, dimenhydrinate, or meclizine, which may have antiemetic properties

- Beta blockers such as metoprolol for vestibular migraine

- Corticosteroids such as methylprednisolone for inflammatory conditions such as vestibular neuritis or dexamethasone as a second-line agent for Ménière's disease

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided. Several treatments may be necessary, and treatment will generally be repeated until either all symptoms resolve, or no further improvement is apparent.

One possible treatment for hyperacusis is retraining therapy which uses broadband noise. Tinnitus retraining therapy, a treatment originally used to treat tinnitus, uses broadband noise to treat hyperacusis. Pink noise can also be used to treat hyperacusis. By listening to broadband noise at soft levels for a disciplined period of time each day, patients can rebuild (i.e., re-establish) their tolerances to sound.

Another possible treatment is cognitive behavioral therapy (CBT), which may also be combined with retraining therapy.

During MD episodes, medications to reduce nausea are used, as are drugs to reduce the anxiety caused by vertigo.

For longer term treatment to stop progression, the evidence base is weak for all treatments.

Although a causal relation between allergy and Menière's disease is uncertain, medication to control allergies may be helpful.

Diuretics are widely used to manage Ménière's on the theory that it reduces fluid buildup in the ear. Based on evidence from multiple but small clinical trials, diuretics appear to be useful for reducing the frequency of episodes of dizziness, but do not seem to prevent hearing loss.

In cases where there is significant hearing loss and continuing severe episodes of vertigo, a chemical labyrinthectomy, in which a drug (such as gentamicin) that "kills" parts or most of the vestibular apparatus is injected into the middle ear.

While use of physical therapy early after the onset of MD is probably not useful due to the fluctuating disease course, physical therapy to help retraining of the balance system appears to be useful to reduce both subjective and objective deficits in balance over the longer term.

Treatment options that offer “cures” for NIHL are under research and development. Currently there are no commonly used cures, but rather assistive devices and therapies to try and manage the symptoms of NIHL.

Several clinical trials have been conducted to treat temporary NIHL occurring after a traumatic noise event, such as a gunshot or firework. In 2007, individuals with acute acoustic trauma after firecracker exposure were injected intratympanically with a cell permeable ligand, AM-111. The trial found AM-111 to have a therapeutic effect on at least 2 cases of those with acute trauma. Treatment with a combination of prednisolone and piracetam appeared to rescue patients with acute trauma after exposure to gunshots. However, those who received the treatment within an hour of exposure had higher rates of recovery and significantly lower threshold shifts compared to those who received treatment after 1 hour.

Additionally, clinical trials using antioxidants after a traumatic noise event to reduce reactive oxygen species have displayed promising results. Antibiotic injections with allopurinol, lazaroids, α-D-tocopherol, and mannitol were found to reduce the threshold shift after noise exposure. Another antioxidant, Ebselen, has been shown to have promising results for both TTS and PTS. Ebselen mimics gluthathione peroxide, an enzyme that has many functions, including scavenging hydrogen peroxide and reactive oxygen species. After noise exposure, gluthathione peroxide decreases in the ear. An oral administration of ebselen in both preclinical tests on guinea pigs and human trials indicate that noise induced TTS and PTS was reduced.

AIED treatment is a rapidly changing field. Several medical therapies have been proposed in the treatment of AIED, with corticosteroid therapy being the most effective. However, corticosteroid therapy (specifically with prednisone and dexamethasone) has demonstrated limited effectiveness in some patients, suggesting the need for novel treatment methods. The goal of most AIED treatments is to administer corticosteroids over a certain period of time, re-evaluate hearing at each appointment, and eventually taper off corticosteroid administration. Ideally, patients can be tapered off with hearing fully recovered, though this is the least likely outcome. Often, tumor necrosis factor-α (TNF-α) inhibitors must be administered alongside corticosteroids to achieve a favorable outcome and eventual end to corticosteroid treatment. Recent papers have indicated that the TNF-α inhibitor, infliximab, has the potential to allow for sustained patient improvement and alleviation of symptoms.

Cytotoxic agents such as cyclophosphamide and methotrexate have been used in AIED treatment in the past; however, findings have suggested limited symptom alleviation from these drugs.

Treatment modalities fall into three categories: pharmacological, surgical, and management. As SNHL is a physiologic degradation and considered permanent, there are as of this time, no approved or recommended treatments.

There have been significant advances in identification of human deafness genes and elucidation of their cellular mechanisms as well as their physiological function in mice. Nevertheless, pharmacological treatment options are very limited and clinically unproven. Such pharmaceutical treatments as are employed are palliative rather than curative, and addressed to the underlying cause if one can be identified, in order to avert progressive damage.

Profound or total hearing loss may be amenable to management by cochlear implants, which stimulate cochlear nerve endings directly. A cochlear implant is surgical implantation of a battery powered electronic medical device in the inner ear. Unlike hearing aids, which make sounds louder, cochlear implants do the work of damaged parts of the inner ear (cochlea) to provide sound signals to the brain. These consist of both internal implanted electrodes and magnets and external components. The quality of sound is different than natural hearing but may enable the recipient to better recognize speech and environmental sounds.

Because of risk and expense, such surgery is reserved for cases of severe and disabling hearing impairment

Management of sensorineural hearing loss involves employing strategies to support existing hearing such as lip-reading, enhanced communication etc. and amplification using hearing aids. Hearing aids are specifically tuned to the individual hearing loss to give maximum benefit.

Treatment with the steroid "prednisone" and the antiviral drug "acyclovir 800mg 5 times a day" is controversial, with some studies showing to achieve complete recovery in patients if started within the first three days of facial paralysis, with chances of recovery decreasing as treatment was delayed. Delay of treatment may result in permanent facial nerve paralysis. However, some studies demonstrate that even when steroids are started promptly, only 22% of all patient achieve full recovery of facial paralysis.

Treatment apparently has no effect on the recovery of hearing loss. Diazepam is sometimes used to treat the vertigo.

About half of people with SSNHL will recover some or all of their hearing spontaneously, usually within one to two weeks from onset. Eighty-five percent of those who receive treatment from an otolaryngologist (sometimes called an ENT) will recover some of their hearing.

- vitamins and antioxidants

- vasodilators

- betahistine (Betaserc), an anti-vertigo drug

- hyperbaric oxygen

- anti-inflammatory agents, primarily oral corticosteroids such as prednisone, methylprednisone

- Intratympanic administration - Gel formulations are under investigation to provide more consistent drug delivery to the inner ear. Local drug delivery can be accomplished through intratympanic administration, a minimally invasive procedure where the ear drum is anesthetized and a drug is administered into the middle ear. From the middle ear, a drug can diffuse across the round window membrane into the inner ear. Intratympanic administration of steroids may be effective for sudden sensorineural hearing loss for some patients, but high quality clinical data has not been generated. Intratympanic administration of an anti-apoptotic peptide (JNK inhibitor) is currently being evaluated in late-stage clinical development.

Earlier workers suggested the use of calcium fluoride; now sodium fluoride is the preferred compound. Fluoride ions inhibit the rapid progression of disease. In the otosclerotic ear, there occurs formation of hydroxylapatite crystals which lead to stapes (or other) fixation. The administration of fluoride replaces the hydroxyl radical with fluoride leading to the formation of fluorapatite crystals. Hence, the progression of disease is considerably slowed down and active disease process is arrested.

This treatment cannot reverse conductive hearing loss, but may slow the progression of both the conductive and sensorineural components of the disease process. Otofluor, containing sodium fluoride, is one treatment. Recently, some success has been claimed with a second such treatment, bisphosphonate medications that inhibit bone destruction. However, these early reports are based on non-randomized case studies that do not meet standards of clinical trials. There are numerous side-effects to both pharmaceutical treatments, including occasional stomach upset, allergic itching, and increased joint pains which can lead to arthritis. In the worst case, bisphosphonates may lead to osteonecrosis of the auditory canal itself. Finally, neither approach has been proven to be beneficial after the commonly preferred method of surgery has been undertaken.

Although hearing aids cannot prevent, cure or inhibit the progression of otosclerosis, they can help treat the largest symptom, hearing loss. Hearing aids can be tuned to specific frequency losses. However, due to the progressive nature of this condition, use of a hearing aid is palliative at best. Without eventual surgery, deafness is likely to result.

A trial of the anticonvulsant drug carbamazepine is common for patients diagnosed with GN. For patients who do not tolerate or respond to carbamazepine, alternative drugs include oxcarbazepine, gabapentin, phenytoin, lamotrigine, and baclofen. In addition, tricyclics (e.g., amitriptyline) and pregabalin are useful in other types of neuropathic pain.

Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.

There is no established treatment for visual snow. It is difficult to resolve visual snow with treatment, but it is possible to reduce symptoms and improve quality of life through treatment.

Medications that may be used include lamotrigine, acetazolamide, or verapamil. But these do not always result in benefits.

At present, presbycusis, being primarily sensorineural in nature, cannot be prevented, ameliorated or cured. Treatment options fall into three categories: pharmacological, surgical and management.

- There are no approved or recommended pharmaceutical treatments for presbycusis.

These are surgically implanted hearing aids inserted onto the middle ear. These aids work by directly vibrating the ossicles, and are cosmetically favorable due to their hidden nature.

As of 2012 there has only been one small-scale study comparing CROS systems.

One study of the BAHA system showed a benefit depending on the patient's transcranial attenuation. Another study showed that sound localisation was not improved, but the effect of the head shadow was reduced.

There are many methods of attempting to reduce the risk of AS. Several devices attempt to remove potentially harmful sound signals by digital signal processing. None has yet been shown to be fully effective. Devices which solely limit noise levels to about 85 dB have been shown in field trials to be ineffective (data from these trials has not been released into the public domain). Limiting background noise and office stress may also reduce the chance of an Acoustic Shock. Proper use of the headset and preventing mobile phones from being used in call centers reduces the chance of feedback.

Another treatment option for an acoustic neuroma is radiation. Stereotactic radiation can be delivered as single fraction stereotactic radiosurgery (SRS) or as multi-session fractionated stereotactic radiotherapy (FSR). Both techniques are performed in the outpatient setting, not requiring general anesthesia or a hospital stay. The purpose of these techniques is to arrest the growth of the tumor. This treatment has not been well studied and thus it is unclear if it is better than observation or surgery.

All types of radiation therapy for acoustic neuromas may result in "tumor control" in which the tumor cells die and necrosis occurs. Tumor control means that the tumor growth may slow or stop and, in some cases, the tumor may shrink in size. Acoustic neuroma tumors have been completely eliminated by radiation treatments in almost no cases. In other words, radiation cannot remove the tumor like microsurgery would. Tumors under 2.5 - 3.0 cm, without significant involvement of the brainstem, are more favorable for radiation treatment. Side effects can occur when the brainstem is irradiated and in some cases of large tumors, radiation is suggested against.

In single dose treatments, hundreds of small beams of radiation are aimed at the tumor. This results in a concentrated dose of radiation to the tumor and avoids exposure of surrounding brain tissues to the radiation. Many patients have been successfully treated this way. Facial weakness or numbness, in the hands of experienced radiation physicians, occurs in only a small percent of cases. Hearing can be preserved in some cases.

The multi-dose treatment, FSR, delivers smaller doses of radiation over a period of time, requiring the patient to return to the treatment location on a daily basis, from 3 to 30 times, generally over several weeks. Each visit lasts a few minutes and most patients are free to go about their daily business before and after each treatment session. Early data indicates that FSR may result in better hearing preservation when compared to single-session SRS.

Radiated patients require lifetime follow-up with MRI scans. Follow-up after SRS and FSR typically involves an MRI scan and audiogram at six months, one year, then yearly for several years, then every second or third year indefinitely to make sure the tumor does not start to grow again. Patients should understand there have been rare reports of malignant degeneration (a benign tumor becoming malignant) after radiotherapy. In some cases the tumor does not die and continues to grow. In those instances, another treatment is necessary - either microsurgery or sometimes another dose of radiation.

Studies are beginning to appear for the other modalities. All of the techniques use computers to create three dimensional models of the tumor and surrounding neural structures. Radiation physicists then create dosimetry maps showing the level of radiation to be received by the tumor and the normal tissues. Surgeons, radiation therapists and physicists then modify the dosimetry to maximize tumor doses and minimize radiation toxicity to surrounding normal tissues. Treatments generally last 30–60 minutes. Just like for surgery, the experience of the team in treating acoustic neuromas with all modalities (surgery and radiation) can affect outcomes.

There are a multitude of studies supporting short-term (<5 yrs.) and longer-term (over 10 yrs.) tumor control with radiation. Unfortunately, as is the case with microsurgical studies, most have inconsistent follow-up to draw definitive conclusions.

Historically, to temporarily alleviate symptoms, patients have tried positional maneuvers, such as tilting their head to one side or upside down, lie down on their backs, or sit in a chair with their head between their knees. Similarly, a routine of lying down four times per day with legs elevated to around 20 inches for at least two weeks has been attempted as well. Depending on the underlying cause of the disorder, the individual may need to remove caffeine from their diet, reduce exercise, or gain weight. It may be the case that the symptoms are induced by anxiety; anxiolytic drugs or supplements (e.g., GABA) combined with the removal of caffeine from the diet could offer a simple strategy to determine if anxiety is the root cause.

Estrogen (Premarin) nasal drops or saturated potassium iodide have been used to induce edema of the eustachian tube opening. Nasal medications containing diluted hydrochloric acid, chlorobutanol, and benzyl alcohol have been reported to be effective in some patients, with few side effects. Food and Drug Administration approval is still pending, however.

In extreme cases surgical intervention may attempt to restore the Eustachian tube tissues with fat, gel foam, or cartilage or scar it closed with cautery. These methods are not always successful.

No specific treatment may be available, but withdrawal of the ototoxic drug may be warranted when the consequences of doing so are less severe than those of the ototoxicity.

Ototoxic monitoring during exposure is recommended by the American Academy of Audiology to allow for proper detection and possible prevention or rehabilitation of the hearing loss through a cochlear implant or hearing aid. Monitoring can be completed through performing otoacoustic emissions testing or high frequency audiometry. Successful monitoring includes a baseline test before, or soon after, exposure to the ototoxin. Follow-up testing is completed in increments after the first exposure, throughout the cessation of treatment. Shifts in hearing status are monitored and relayed to the prescribing physician to make treatment decisions.

It is difficult to distinguish between nerve damage and structural damage due to similarity of the symptoms. Diagnosis of ototoxicity typically results from ruling out all other possible sources of hearing loss and is often the catchall explanation for the symptoms. Treatment options vary depending on the patient and the diagnosis. Some patients experience only temporary symptoms that do not require drastic treatment while others can be treated with medication. Physical therapy may prove useful for regaining balance and walking abilities. Cochlear implants are sometimes an option to restore hearing. Such treatments are typically taken to comfort the patient, not to cure the disease or damage caused by ototoxicity. There is no cure or restoration capability if the damage becomes permanent, although cochlear nerve terminal regeneration has been observed in chickens, which suggests that there may be a way to accomplish this in humans.

Given the unknown nature of MES, treatments have been largely dependent on an individual basis. Treatments can vary from being as little as self-reassurance to pharmaceutical medications.

Medications can be helpful, such as antipsychotics, benzodiazepines or antiepileptics, but there is very limited evidence for this. Some case studies have found that switching to a prednisolone steroid after a betamethasone steroid which caused MES helped alleviate hallucinations or the use of the acetylcholinesterase inhibitor, Donepezil, have also found that it successfully treated an individual's MES. However, because of the heterogeneous etiology, these methods cannot be applied as general treatment.

Other than treatment by medicinal means, individuals have also successfully alleviated musical hallucinations by cochlear implants, listening to different songs via an external source, or by attempting to block them through mental effort, depending on how severe their condition is.