Treating auditory verbal agnosia with intravenous immunoglobulin (IVIG) is controversial because of its inconsistency as a treatment method. Although IVIG is normally used to treat immune diseases, some individuals with auditory verbal agnosia have responded positively to the use of IVIG. Additionally, patients are more likely to relapse when treated with IVIG than other pharmacological treatments. IVIG is, thus, a controversial treatment as its efficacy in treating auditory verbal agnosia is dependent upon each individual and varies from case to case.

In incidents where tumors and their pressure effects are the cause of pure word deafness, removal of the tumor has been shown to allow for the return of most auditory verbal comprehension.

Currently, no forms of treatment have proven effective in treating amusia. One study has shown tone differentiation techniques to have some success, however future research on treatment of this disorder will be necessary to verify this technique as an appropriate treatment.

There is no treatment, surgical or otherwise, for hearing loss due to the most common causes (age, noise, and genetic defects). For a few specific conditions, surgical intervention can provide a remedy:

- surgical correction of superior canal dehiscence

- myringotomy, surgical insertion of drainage ventilation tubes in the tympanic membrane. Such placement is usually temporary until the underlying pathology (infection or other inflammation) can be resolved.

- radiotherapy or surgical excision of vestibular schwannoma or acoustic neuroma, though, in most cases, it is unlikely that hearing will be preserved

- Stapedectomy and stapedotomy for otosclerosis - replacement or reshaping of the stapes bone of the middle ear can restore hearing in cases of conductive hearing loss

Surgical and implantable hearing aids are an alternative to conventional external hearing aids.

If the ear is dry and not infected, an air conduction aid could be tried; if the ear is draining, a direct bone condition hearing aid is often the best solution. If the conductive part of the hearing loss is more than 30–35 dB, an air conduction device could have problems overcoming this gap. A bone-anchored hearing aid could, in this situation, be a good option.

The active bone conduction hearing implant Bonebridge is also an option. This implant is invisible under the intact skin and therefore minimises the risk of skin irritations.

Cochlear implants improve outcomes in people with hearing loss in either one or both ears. They work by artificial stimulation of the cochlear nerve by providing an electric impulse substitution for the firing of hair cells. They are expensive, and require programming along with extensive training for effectiveness.

Cochlear implants as well as bone conduction implants can help with single sided deafness.

Middle ear implants or bone conduction implants can help with conductive hearing loss.

People with cochlear implants are at a higher risk for bacterial meningitis. Thus, meningitis vaccination is recommended. People who have hearing loss, especially those who develop a hearing problem in childhood or old age, may need support and technical adaptations as part of the rehabilitation process. Recent research shows variations in efficacy but some studies show that if implanted at a very young age, some profoundly impaired children can acquire effective hearing and speech, particularly if supported by appropriate rehabilitation.

Auditory perception can improve with time.There seems to be a level of neuroplasticity that allows patients to recover the ability to perceive environmental and certain musical sounds. Patients presenting with cortical hearing loss and no other associated symptoms recover to a variable degree, depending on the size and type of the cerebral lesion. Patients whose symptoms include both motor deficits and aphasias often have larger lesions with an associated poorer prognosis in regard to functional status and recovery.

Cochlear or auditory brainstem implantation could also be treatment options. Electrical stimulation of the peripheral auditory system may result in improved sound perception or cortical remapping in patients with cortical deafness. However, hearing aids are an inappropriate answer for cases like these. Any auditory signal, regardless if has been amplified to normal or high intensities, is useless to a system unable to complete its processing. Ideally, patients should be directed toward resources to aid them in lip-reading, learning American Sign Language, as well as speech and occupational therapy. Patients should follow-up regularly to evaluate for any long-term recovery.

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.

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 depends on the specific cause if known as well as the extent, type and configuration of the hearing loss. Most hearing loss, that resulting from age and noise, is progressive and irreversible, and there are currently no approved or recommended treatments; management is by hearing aid. A few specific kinds of hearing loss are amenable to surgical treatment. In other cases, treatment is addressed to underlying pathologies, but any hearing loss incurred may be permanent.

There are a number of devices that can improve hearing in those who are deaf or hard of hearing or allow people with these conditions to manage better in their lives.

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.

In cases where the causes are environmental, the treatment is to eliminate or reduce these causes first of all, and then to fit patients with a hearing aid, especially if they are elderly. When the loss is due to heredity, total deafness is often the end result. On the one hand, persons who experience gradual deterioration of their hearing are fortunate in that they have learned to speak. Ultimately the affected person may bridge communication problems by becoming skilled in sign language, speech-reading, using a hearing aid, or accepting elective surgery to use a prosthetic devices such as a cochlear implant.

Treatment of Foix–Chavany–Marie syndrome depends on the onset of symptoms and involves a multidisciplinary approach. Drugs are used in neurological recovery depending on the etiological classification of FCMS. FCMS caused by epilepsy, specifically resulting in the development of lesions in the bilateral and subcortical regions of the brain can be treated using antiepileptic drugs to reverse abnormal EEG changes and induce complete neurological recovery. In addition, a hemispherectomy can be performed to reverse neurological deficits and control the seizures. This procedure can result in a complete recovery from epileptic seizures. Physical therapy is also used to manage symptoms and improve quality of life. Classical FCMS resulting in the decline of ones ability to speak and swallow can be treated using neuromuscular electrical stimulation and traditional dysphagia therapy. Speech therapy further targeting dysphagia can strengthen oral musculature using modified feeding techniques and postures. Therapeutic feedings include practicing oral and lingual movements using ice chips. In addition, different procedures can be performed by a neurosurgeon to alleviate some symptoms.

To date, there is no successful method of treatment that "cures" musical hallucinations. There have been successful therapies in single cases that have ameliorated the hallucinations. Some of these successes include drugs such as neuroleptics, antidepressants, and certain anticonvulsive drugs. A musical hallucination was alleviated, for example, by antidepressant medications given to patients with depression. Sanchez reported that some authors have suggested that the use of hearing aids may improve musical hallucination symptoms. They believed that the external environment influences the auditory hallucinations, showing worsening of symptoms in quieter environments than in noisier ones. Oliver Sacks' patient, Mrs. O'C, reported being in an "ocean of sound" despite being in a quiet room due to a small thrombosis or infarction in her right temporal lobe. After treatment, Mrs. O'C was relinquished of her musical experience but said that, "I do miss the old songs. Now, with lots of them, I can't even recall them. It was like being given back a forgotten bit of my childhood again." Sacks also reported another elderly woman, Mrs. O'M, who had a mild case of deafness and reported hearing musical pieces. When she was treated with anticonvulsive medications, her musical hallucinations ceased but when asked if she missed them, she said "Not on your life."

Palinopsia from cerebrovascular accidents generally resolves spontaneously, and treatment should be focused on the vasculopathic risk factors. Palinopsia from neoplasms, AVMs, or abscesses require treatment of the underlying condition, which usually also resolves the palinopsia. Palinopsia due to seizures generally resolves after correcting the primary disturbance and/or treating the seizures. In persistent hallucinatory palinopsia, a trial of an anti-epileptic drug can be attempted. Anti-epileptics reduce cortical excitability and could potentially treat palinopsia caused by cortical deafferentation or cortical irritation. Patients with idiopathic hallucinatory palinopsia should have close follow-up.

Cortical deafness is a rare form of sensorineural hearing loss caused by damage to the primary auditory cortex. Cortical deafness is an auditory disorder where the patient is unable to hear sounds but has no apparent damage to the anatomy of the ear (see auditory system), which can be thought of as the combination of auditory verbal agnosia and auditory agnosia. Patients with cortical deafness cannot hear any sounds, that is, they are not aware of sounds including non-speech, voices, and speech sounds. Although patients appear and feel completely deaf, they can still exhibit some reflex responses such as turning their head towards a loud sound.

Cortical deafness is caused by bilateral cortical lesions in the primary auditory cortex located in the temporal lobes of the brain. The ascending auditory pathways are damaged, causing a loss of perception of sound. Inner ear functions, however, remains intact. Cortical deafness is most often cause by stroke, but can also result from brain injury or birth defects. More specifically, a common cause is bilateral embolic stroke to the area of Heschl's gyri. Cortical deafness is extremely rare, with only twelve reported cases. Each case has a distinct context and different rates of recovery.

It is thought that cortical deafness could be a part of a spectrum of an overall cortical hearing disorder. In some cases, patients with cortical deafness have had recovery of some hearing function, resulting in partial auditory deficits such as auditory verbal agnosia. This syndrome might be difficult to distinguish from a bilateral temporal lesion such as described above.

No specific treatment exists for Pendred syndrome. Speech and language support and hearing aids are important. Cochlear implants may be needed if the hearing loss drops to severe to profound levels and can improve language skills. If thyroid hormone levels are decreased, thyroid hormone supplements may be required. Patients are advised to take precautions against head injury.

Those who lose their hearing later in life, such as in late adolescence or adulthood, face their own challenges. For example, they must adjust to living with the adaptations that make it possible for them to live independently. They may have to adapt to using hearing aids or a cochlear implant, develop speech-reading skills, and/or learn sign language. The affected person may need to use a TTY, a videophone, an interpreter, or relay service to communicate over the telephone. Loneliness and depression can arise as a result of isolation (from the inability to communicate with friends and loved ones) and difficulty in accepting their disability. The challenge is made greater by the need for those around them to adapt to the person's hearing loss.

Hearing aids and cochlear implants may make the child able to hear sounds in their hearing range—but they don't restore normal hearing. Cochlear implants can stimulate the auditory nerve directly to restore some hearing, but the sound quality isn't that of a normal hearing ear, suggesting that deafness cannot be fully overcome by medical devices. Some say that the benefits and safety of cochlear implants continues to grow, especially when children with implants receive a lot of oral educational support. It is a goal for some audiologists to test and fit a deaf child with a cochlear implant by six months of age, so that they don't get behind in learning language. In fact, there are expectations that if children get fit for implants early enough, they can acquire verbal language skills to the same level as their peers with normal hearing.

Specific and accepted scientific treatment for PCA has yet to be discovered; this may be due to the rarity and variations of the disease. At times PCA patients are treated with prescriptions originally created for treatment of AD such as, cholinesterase inhibitors, Donepezil, Rivastigmine and Galantamine, and Memantine. Antidepressant drugs have also provided some positive effects.

Patients may find success with non-prescription treatments such as psychological treatments. PCA patients may find assistance in meeting with an occupational therapist or sensory team for aid in adapting to the PCA symptoms, especially for visual changes. People with PCA and their caregivers are likely to have different needs to more typical cases of Alzheimer's disease, and may benefit from specialized support groups such as the PCA Support Group based at University College London, or other groups for young people with dementia. No study to date has been definitive to provide accepted conclusive analysis on treatment options.

The prognosis of a patient with acquired cortical blindness depends largely on the original cause of the blindness. For instance, patients with bilateral occipital lesions have a much lower chance of recovering vision than patients who suffered a transient ischemic attack or women who experienced complications associated with eclampsia. In patients with acquired cortical blindness, a permanent complete loss of vision is rare. The development of cortical blindness into the milder cortical visual impairment is a more likely outcome. Furthermore, some patients regain vision completely, as is the case with transient cortical blindness associated with eclampsia and the side effects of certain anti-epilepsy drugs.

Recent research by Krystel R. Huxlin and others on the relearning of complex visual motion following V1 damage has offered potentially promising treatments for individuals with acquired cortical blindness. These treatments focus on retraining and retuning certain intact pathways of the visual cortex which are more or less preserved in individuals who sustained damage to V1. Huxlin and others found that specific training focused on utilizing the "blind field" of individuals who had sustained V1 damage improved the patients' ability to perceive simple and complex visual motion. This sort of 'relearning' therapy may provide a good workaround for patients with acquired cortical blindness in order to better make sense of the visual environment.

Beat deafness is a form of congenital amusia characterized by a person's inability to distinguish musical rhythm or move in time to it.

Prelingual hearing loss can be either acquired, meaning it occurred after birth due to illness or injury, or it can be congenital, meaning it was present at birth. Congenital hearing loss can be caused by genetic or nongenetic factors. The nongenetic factors account for about one fourth of the congenital hearing losses in infants. These factors could include: Maternal infections, such as rubella, cytomegalovirus, or herpes simplex virus, lack of oxygen, maternal diabetes, toxemia during pregnancy, low birth weight, prematurity, birth injuries, toxins including drugs and alcohol consumed by the mother during pregnancy, and complications associated with the Rh factor in the blood/jaundice. Genetic factors account for over half of the infants with congenital hearing loss. Most of these are caused by an autosomal recessive hearing loss or an autosomal dominant hearing loss. Autosomal recessive hearing loss is when both parents carry the recessive gene, and pass it on to their child. The autosomal dominant hearing loss is when an abnormal gene from one parent is able to cause hearing loss even though the matching gene from the other parent is normal.

Phonagnosia (from Ancient Greek φωνή "phone", "voice" and γνῶσις "gnosis", "knowledge") is a type of agnosia, or loss of knowledge, that involves a disturbance in the recognition of familiar voices and the impairment of voice discrimination abilities in which the affected individual does not suffer from comprehension deficits. Phonagnosia is an auditory agnosia, an acquired auditory processing disorder resulting from brain damage, other auditory agnosias include cortical deafness and auditory verbal agnosia also known as pure word deafness.

Since people suffering from phonagnosia do not suffer from aphasia, it is suggested that the structures of linguistic comprehension are functionally separate from those of the perception of the identity of the speaker who produced it.

Phonagnosia is the auditory equivalent of prosopagnosia. Unlike Prosopagnosia, investigations of phonagnosia have not been extensively pursued. Phonagnosia was first described by a study by Van Lancker and Cantor in 1982. The subjects in this study were asked to identify which of four names or faces matched a specific famous voice. The subjects could not complete the task. Since then, there have been a couple studies done on patients with phonagnosia. The clinical and radiologic findings with computerized tomographic scans cat scan in these cases suggest that recognition of familiar voices is impaired by damage to the inferior and parietal regions of the right hemisphere while voice discrimination is impaired by temporal lobe damage of either hemisphere. These studies have also shown evidence for a double dissociation between voice recognition and voice discrimination. Some patients will perform normally on the discrimination tasks but poorly on the recognition tasks; whereas the other patients will perform normally on the recognition tasks but poorly on the discrimination tasks. Patients did not perform poorly on both tasks.

Associative phonagnosia is a form of phonagnosia that develops with dementia or other focal neurodegenerative disorders. Some research has led to questions of other impairments in phonagnosics. Recently, studies have shown that phonagnosics also have trouble in recognizing the sounds of familiar instruments. As it is with voices, they also show deficiency in distinguishing between sounds from different instruments. Although the disability is shown, phonagnosics are much less affected in this area of sound discrimination. In distinguishing voices, it is a complete agnosia, but this is not the case for musical instrument sounds, as they can correctly identify some of them. Controversy arises in that not all phonagnosics exhibit these symptoms, and so not all researchers agree that it should be attributed to the damage suffered that causes phonagnosia. Much debate has arisen over the fact that it seems that separate areas of the brain are utilized to handle information from language and music. This has led some researchers to skeptically consider this impairment as a clear symptom of the disorder. Again, more research is needed to create a clearer conclusion.

An interesting attribute that phonagnosics possess is that they can correctly detect emotions in voices when someone talks to them. They can also correctly match an emotion with a facial expression. Although surprising, this finding is sensible because it is known and well agreed upon that the limbic system, involved in expressing emotions and detecting emotions of others, is a separate system within the brain. The limbic system is made up of several brain structures including the hippocampus, amygdala, anterior thalamic nuclei, septum, limbic cortex and fornix.

Presently, there is no therapy or treatment for phonagnosia. Clearly, more research is needed to accomplish the feat of developing treatment for the disorder. The lack of treatment stems from the lack of knowledge about the disorder. Increased research will reveal vital information needed to formulate effective treatments and therapies.

Research needs to be performed on the efficacy of the various pharmaceuticals for treating illusory palinopsia. It is unclear if the symptoms' natural history and treatment are influenced by the cause. It is also not clear if there is treatment efficacy overlap for illusory palinopsia and the other co-existing diffuse persistent illusory phenomenon such as visual snow, oscillopsia, dysmetropsia, and halos.

Future advancements in fMRI could potentially further our understanding of hallucinatory palinopsia and visual memory. Increased accuracy in fMRI might also allow for the observation of subtle metabolic or perfusional changes in illusory palinopsia, without the use of ionizing radiation present in CT scans and radioactive isotopes. Studying the psychophysics of light and motion perception could advance our understanding of illusory palinopsia, and vice versa. For example, incorporating patients with visual trailing into motion perception studies could advance our understanding of the mechanisms of visual stability and motion suppression during eye movements (e.g. saccadic suppression).

Over the past decade, much has been discovered about amusia. However, there remains a great deal more to learn. While a method of treatment for people with amusia has not been defined, tone differentiation techniques have been used on amusic patients with some success. It was found with this research that children reacted positively to these tone differentiation techniques, while adults found the training annoying. However, further research in this direction would aid in determining if this would be a viable treatment option for people with amusia. Additional research can also serve to indicate which processing component in the brain is essential for normal music development. Also, it would be extremely beneficial to investigate musical learning in relation to amusia since this could provide valuable insights into other forms of learning disabilities such as dysphasia and dyslexia.

Intoxication accounts for a small percentage of musical hallucination cases. Intoxication leads to either withdrawal or inflammatory encephalopathy, which are major contributors to musical hallucinations. Some of the drugs that have been found to relate to musical hallucinations include salicylates, benzodiazepines, pentoxifylline, propranolol, clomipramine, amphetamine, quinine, imipramine, a phenothiazine, carbamazepine, marijuana, paracetamol, phenytoin, procaine, and alcohol. General anesthesia has also been association with musical hallucinations.

In a case study by Gondim et al. 2010, a seventy–seven-year-old woman with Parkinson's disease (PD) was administered amantadine after a year of various other antiparkinsonian treatments. Two days into her treatment, she started to experience musical hallucinations, which consisted of four musical pieces. The music persisted until three days after cessation of the drug. Although the patient was taking other medications at the same time, the timing of onset and offset suggested that amantadine either had a synergistic effect with the other drugs or simply caused the hallucinations. Although the case wasn't specific to intoxication, it leads to the idea that persons with PD who are treated with certain drugs can experience musical hallucinations.