Various strategies may be used to manage tympanic membrane retraction, with the aims of preventing or relieving hearing loss and cholesteatoma formation.

While there is no cure, most people with tinnitus get used to it over time; for a minority, it remains a significant problem.

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.

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.

Management falls into three modalities: surgical treatment, pharmaceutical treatment, and supportive, depending on the nature and location of the specific cause.

In cases of infection, antibiotics or antifungal medications are an option. Some conditions are amenable to surgical intervention such as middle ear fluid, cholesteatoma, otosclerosis. If conductive hearing loss is due to head trauma, surgical repair is an option. If absence or deformation of ear structures cannot be corrected, or if the patient declines surgery, hearing aids which amplify sounds are a possible treatment option. Bone conduction hearing aids are useful as these deliver sound directly, through bone, to the cochlea or organ of hearing bypassing the pathology. These can be on a soft or hard headband or can be inserted surgically, a bone anchored hearing aid, of which there are several types. Conventional air conduction hearing aids can also be used.

As retraction pockets may remain stable or resolve spontaneously, it may be appropriate to observe them for a period of time before considering any active treatment.

If there is an underlying cause, treating it may lead to improvements. Otherwise, the primary treatment for tinnitus is talk therapy and sound therapy; there are no effective medications.

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.

Presbycucis is the leading cause of SNHL and is progressive and nonpreventable, and at this time, we do not have either somatic or gene therapy to counter heredity-related SNHL. But other causes of acquired SNHL are largely preventable, especially nosocusis type causes. This would involve avoiding environmental noise, and traumatic noise such as rock concerts and nightclubs with loud music. Use of noise attenuation measures like acoustic ear plugs is an alternative.

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.

Cholesteatoma is a persistent disease. Once the diagnosis of cholesteatoma is made in a patient who can tolerate a general anesthetic, the standard treatment is to surgically remove the growth.

The challenge of cholesteatoma surgery is to permanently remove the cholesteatoma whilst retaining or reconstructing the normal functions of the structures housed within the temporal bone.

The general objective of cholesteatoma surgery has two parts. It is both directed against the underlying pathology and directed towards maintaining the normal functions of the temporal bone. These aims are conflicting and this makes cholesteatoma surgery extremely challenging.

Sometimes, the situation results in a clash of surgical aims. The need to fully remove a progressive disease like cholesteatoma is the surgeon's first priority. Preservation of hearing is secondary to this primary aim. If the disease can be removed easily so that there is no increased risk of residual disease, then the ossicles may be preserved. If the disease is difficult to remove, so that there is an increased risk of residual disease, then removal of involved ossicles in order to fully clear cholesteatoma has generally been regarded as necessary and reasonable.

In other words, the aims of cholesteatoma treatment form a hierarchy. The paramount objective is the complete removal of cholesteatoma. The remaining objectives, such as hearing preservation, are subordinate to the need for complete removal of cholesteatoma. This hierarchy of aims has led to the development of a wide range of strategies for the treatment of cholesteatoma.

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.

Myringosclerosis seems to be more common than tympanosclerosis. Most research has not been conducted upon the general, healthy population, but rather those with otitis media or patients who have had tympanostomy tubes in prior procedures. Of the children studied who had 'glue ear', and who were treated with tympanostomy tubing, 23-40% of cases had tympanosclerosis. One study suggested that people with atherosclerosis were more likely to have tympanosclerosis than otherwise healthy individuals.

Hearing aids are a common treatment for hearing loss disorders. A more specific treatment is surgical, involving excision of the sclerotic areas and then further repair of the ossicular chain. There are several techniques, sometimes involving two surgeries; success rates are, however, variable. Damage to the inner ear as a result of surgical procedures is a possible and serious concern, as it can result in forms of sensorineural deafness.

The variation in technique in cholesteatoma surgery results from each surgeon's judgment whether to retain or remove certain structures housed within the temporal bone in order to facilitate the removal of cholesteatoma. This typically involves some form of mastoidectomy which may or may not involve removing the posterior ear canal wall and the ossicles.

Removal of the canal wall facilitates the complete clearance of cholesteatoma from the temporal bone in three ways:

1. it removes a large surface onto which cholesteatoma may be adherent;

2. it removes a barrier behind which the cholesteatoma may be hidden;

3. it removes an impediment to the introduction of instruments used for the removal of cholesteatoma.

Thus removal of the canal wall provides one of the most effective strategies for achieving the primary aim of cholesteatoma surgery, the complete removal of cholesteatoma. However, there is a trade-off, since the functional impact of canal wall removal is also important.

The removal of the ear canal wall results in:

- a space, the "mastoid cavity", which is less likely than the original ear canal to resist infection;

- exposure of the ossicles, which may allow the subsequent formation of a new cholesteatoma deep to the ossicles. To prevent this, these ossicles must be removed, which may diminish the patient's hearing.

The formation of a mastoid cavity by removal of the canal wall is the simplest and most effective procedure for facilitating the removal of cholesteatoma, but may bestow the most lasting infirmity due to loss of ear function upon the patient treated in this way.

The following strategies are employed to mitigate the effects of canal wall removal:

1. careful design and construction of the mastoid cavity. This is essential for the health and integrity of the protective sheet of migrating, keratising epithelium which lines the distorted ear canal. This requires the surgeon to saucerise the cavity. A high facial ridge and an inappropriately small cartilaginous meatus are obstructions to epithelial migration and are particularly high risk factors for failure of the self-cleaning mechanism of the external ear.

2. partial obliteration of the mastoid cavity. This can be performed using a wide range of materials. Many of these resorb in time, which means that the long-term results of such surgery are poorer than the short-term results.

3. reconstruction of the ear canal wall. Canal wall reconstruction has been performed using ear canal skin alone, fascia, cartilage, titanium as well as by replacing the original intact wall. If the reconstruction is poorly performed, it may result in a high rate of recurrent cholesteatoma.

4. preservation of the ear canal wall. If poorly performed, it may result in a high rate of both residual and recurrent cholesteatoma.

5. reconstruction of the chain of hearing bones.

Clearly, preservation and restoration of ear function at the same time as total removal of cholesteatoma requires a high level of surgical expertise.

Treatment is supportive and consists of management of manifestations. User of hearing aids and/or cochlear implant, suitable educational programs can be offered. Periodic surveillance is also important.

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.

Patients are advised to treat with bed rest and avoiding activities that increase intracranial pressure (i.e. weightlifting, valsalva, scuba diving, flying in airplanes) with the hopes of the membrane healing on their own. Appropriate Physical therapy / vestibular rehabilitation techniques can be helpful in managing symptoms of movement sensitivity.

Third window effect caused by:

- Superior canal dehiscence – which may require surgical correction.

- Widened vestibular aqueducts

Otosclerosis or otospongiosis is an abnormal growth of bone near the middle ear. It can result in hearing loss. The term otosclerosis is something of a misnomer. Much of the clinical course is characterised by lucent rather than sclerotic bony changes, hence it is also known as otospongiosis.

Once diagnosed, the gap in the temporal bone can be repaired by surgical resurfacing of the affected bone or plugging of the superior semicircular canal. These techniques are performed by accessing the site of the dehiscence either via a middle fossa craniotomy or via a canal drilled through the transmastoid bone behind the affected ear. Bone cement has been the material most often used, in spite of its tendency to slippage and resorption, and a consequent high failure rate; recently, soft tissue grafts have been substituted.

People with MD are often advised to reduce their salt intake for similar reasons, but the evidence for this is very poor. Based on the assumption that MD is similar in nature to a migraine, some advise eliminating "migraine triggers" like caffeine. However, the evidence for this is weak.

The strategies for preventing acute external otitis are similar to those for treatment.

- Avoid inserting "anything" into the ear canal: use of cotton buds or swabs is the most common event leading to acute otitis externa.

- Most normal ear canals have a self-cleaning and self-drying mechanism, the latter by simple evaporation.

- After prolonged swimming, a person prone to external otitis can dry the ears using a small battery-powered ear dryer, available at many retailers, especially shops catering to watersports enthusiasts. Alternatively, drops containing dilute acetic acid (vinegar diluted 3:1) or Burow's solution may be used. It is especially important NOT to instrument ears when the skin is saturated with water, as it is very susceptible to injury, which can lead to external otitis.

- Avoid swimming in polluted water.

- Avoid washing hair or swimming if very mild symptoms of acute external otitis begin

- Although the use of earplugs when swimming and shampooing hair may help prevent external otitis, there are important details in the use of plugs. Hard and poorly fitting ear plugs can scratch the ear canal skin and set off an episode. When earplugs are used during an acute episode, either disposable plugs are recommended, or used plugs must be cleaned and dried properly to avoid contaminating the healing ear canal with infected discharge.

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.

When diagnosing, PLF should be differentiated from Ménière's disease. Tympanostomy has been reported to be a way to diagnose and cure PLF.