Universal Newborn Hearing Screenings (UNHS) is mandated in a majority of the United States. Auditory neuropathy is sometimes difficult to catch right away, even with these precautions in place. Parental suspicion of a hearing loss is a trustworthy screening tool for hearing loss, too; if it is suspected, that is sufficient reason to seek a hearing evaluation from an audiologist.

In most parts of Australia, hearing screening via AABR testing is mandated, meaning that essentially all congenital (i.e., not those related to later onset degenerative disorders) auditory neuropathy cases should be diagnosed at birth.

A number of computer-based auditory training programs exist for children with generalized Auditory Processing Disorders (APD). In the visual system, it has been proven that adults with amblyopia can improve their visual acuity with targeted brain training programs (perceptual learning). A focused perceptual training protocol for children with amblyaudia called Auditory Rehabilitation for Interaural Asymmetry (ARIA) was developed in 2001 which has been found to improve dichotic listening performance in the non-dominant ear and enhance general listening skills. ARIA is now available in a number of clinical sites in the U.S., Canada, Australia and New Zealand. It is also undergoing clinical research trials involving electrophysiologic measures and activation patterns acquired through functional magnetic resonance imaging (fMRI) techniques to further establish its efficacy to remediate amblyaudia.

Individuals with conduction aphasia are able to express themselves fairly well, with some word finding and functional comprehension difficulty. Although people with aphasia may be able to express themselves fairly well, they tend to have issues repeating phrases, especially phrases that are long and complex. When asked to repeat something, the patient will be unable to do so without significant difficulty, repeatedly attempting to self-correct ("conduite d'approche"). When asked a question, however, patients can answer spontaneously and fluently.

Several standardized test batteries exist for diagnosing and classifying aphasias. These tests are capable of identifying conduction aphasia with relative accuracy. The Boston Diagnostic Aphasia Examination (BDAE) and the Western Aphasia Battery (WAB) are two commonly used test batteries for diagnosing conduction aphasia. These examinations involve a set of tests, which include asking patients to name pictures, read printed words, count aloud, and repeat words and non-words (such as "shwazel").

A clinical diagnosis of amblyaudia is made following dichotic listening testing as part of an auditory processing evaluation. Clinicians are advised to use newly developed dichotic listening tests that provide normative cut-off scores for the listener's dominant and non-dominant ears. These are the Randomized Dichotic Digits Test and the Dichotic Words Test. Older dichotic listening tests that provide normative information for the right and left ears can be used to supplement these two tests for support of the diagnosis (). If performance across two or more dichotic listening tests is normal in the dominant ear and significantly below normal in the non-dominant ear, a diagnosis of amblyaudia can be made. The diagnosis can also be made if performance in both ears is below normal but performance in the non-dominant ear is significantly poorer, thereby resulting in an abnormally large asymmetry between the two ears. Amblyaudia is emerging as a distinct subtype of auditory processing disorder (APD).

When testing the auditory system, there really is no characteristic presentation on the audiogram.

When diagnosing someone with auditory neuropathy, there is no characteristic level of functioning either. People can present relatively little dysfunction other than problems of hearing speech in noise, or can present as completely deaf and gaining no useful information from auditory signals.

Hearing aids are sometimes prescribed, with mixed success.

Some people with auditory neuropathy obtain cochlear implants, also with mixed success.

Treatment for aphasias is generally individualized, focusing on specific language and communication improvements, and regular exercise with communication tasks. Regular therapy for conduction aphasics has been shown to result in steady improvement on the Western Aphasia Battery. However, conduction aphasia is a mild aphasia, and conduction aphasics score highly on the WAB at baseline.

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.

1. SCAN is the most common tool for diagnosing APD, and it also standardized. It is composed for four subsets: discrimination of monaurally presented single words against background noise, acoustically degraded single words, dichotically presented single words, sentence stimuli. Different versions of the test are used depending on the age of the patient.

2. Random Gap Detection Test (RGDT) is also a standardized test. It assesses an individual’s gap detection threshold of tones and white noise. The exam includes stimuli at four different frequencies (500, 1000, 2000, and 4000 Hz) and white noise clicks of 50 ms duration. It is a useful test because it provides an index of auditory temporal resolution. In children, an overall gap detection threshold greater than 20 ms means they have failed.

3. Gaps in Noise Test (GIN) also measures temporal resolution by testing the patient's gap detection threshold in white noise.

4. Pitch Patterns Sequence Test (PPT) and Duration Patterns Sequence Test (DPT) measure auditory pattern identification. The PPS has s series of three tones presented at either of two pitches (high or low). Meanwhile, the DPS has a series of three tones that vary in duration rather than pitch (long or short). Patients are then asked to describe the pattern of pitches presented.

Sign language therapy has been identified as one of the top five most common treatments for auditory verbal agnosia. This type of therapy is most useful because, unlike other treatment methods, it does not rely on fixing the damaged areas of the brain. This is particularly important with AVA cases because it has been so hard to identify the causes of the agnosia in the first place, much less treat those areas directly. Sign language therapy, then, allows the person to cope and work around the disability, much in the same way it helps deaf people. In the beginning of therapy, most will work on identifying key objects and establishing an initial core vocabulary of signs. After this, the patient graduates to expand the vocabulary to intangible items or items that are not in view or present. Later, the patient learns single signs and then sentences consisting of two or more signs. In different cases, the sentences are first written down and then the patient is asked to sign them and speak them simultaneously. Because different AVA patients vary in the level of speech or comprehension they have, sign language therapy learning order and techniques are very specific to the individual's needs.

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.

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.

In human neuroanatomy, brainstem auditory evoked potentials (BAEPs), also called brainstem auditory evoked responses (BAERs), are very small auditory evoked potentials in response to an auditory stimulus, which are recorded by electrodes placed on the scalp. They reflect neuronal activity in the auditory nerve, cochlear nucleus, superior olive, and inferior colliculus of the brainstem. They typically have a response latency of no more than six milliseconds with an amplitude of approximately one microvolt.

Due to their small amplitude, 500 or more repetitions of the auditory stimulus are required in order to average out the random background electrical activity. Although it is possible to obtain a BAEP to a pure tone stimulus in the hearing range a more effective auditory stimulus contains a range of frequencies in the form of a short sharp click.

Long and Allen were the first to report the abnormal BAEPs in an alcoholic woman who recovered from acquired central hypoventilation syndrome. These investigators hypothesized that their patient's brainstem was poisoned, but not destroyed, by her chronic alcoholism.

Psychopharmacological treatments include anti-psychotic medications. Psychology research shows that first step in treatment is for the patient to realize that the voices they hear are creation of their own mind. This realization is argued to allow patients to reclaim a measure of control over their lives. Some additional psychological interventions might allow for the process of controlling these phenomena of auditory hallucinations but more research is needed.

Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but a neurological inability of the brain to process sound meaning. It is a disruption of the "what" pathway in the brain. Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it "was" a lion creating the noise. Auditory agnosia is caused by damage to the secondary and tertiary auditory cortex of the temporal lobe of the brain.

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.

APD is a difficult disorder to detect and diagnose. The subjective symptoms that lead to an evaluation for APD include an intermittent inability to process verbal information, leading the person to guess to fill in the processing gaps. There may also be disproportionate problems with decoding speech in noisy environments.

APD has been defined anatomically in terms of the integrity of the auditory areas of the nervous system. However, children with symptoms of APD typically have no evidence of neurological disease and the diagnosis is made on the basis of performance on behavioral auditory tests. Auditory processing is "what we do with what we hear", and in APD there is a mismatch between peripheral hearing ability (which is typically normal) and ability to interpret or discriminate sounds. Thus in those with no signs of neurological impairment, APD is diagnosed on the basis of auditory tests. There is, however, no consensus as to which tests should be used for diagnosis, as evidenced by the succession of task force reports that have appeared in recent years. The first of these occurred in 1996. This was followed by a conference organized by the American Academy of Audiology. Experts attempting to define diagnostic criteria have to grapple with the problem that a child may do poorly on an auditory test for reasons other than poor auditory perception: for instance, failure could be due to inattention, difficulty in coping with task demands, or limited language ability. In an attempt to rule out at least some of these factors, the American Academy of Audiology conference explicitly advocated that for APD to be diagnosed, the child must have a modality-specific problem, i.e. affecting auditory but not visual processing. However, an ASHA committee subsequently rejected modality-specificity as a defining characteristic of auditory processing disorders.

There are three primary distinctions of auditory agnosia that fall into two categories.

Research has shown that PC based spatial hearing training software can help some of the children identified as failing to develop their spatial hearing skills (perhaps because of frequent bouts of otitis media with effusion). Further research is needed to discover if a similar approach would help those over 60 to recover the loss of their spatial hearing. One such study showed that dichotic test scores for the left ear improved with daily training. Related research into the plasticity of white-matter (see Lövdén et al. for example) suggests some recovery may be possible.

Music training leads to superior understanding of speech in noise across age groups and musical experience protects against age-related degradation in neural timing. Unlike speech (fast temporal information), music (pitch information) is primarily processed by areas of the brain in the right hemisphere. Given that it seems likely that the right ear advantage (REA) for speech is present from birth, it would follow that a left ear advantage for music is also present from birth and that MOC efferent inhibition (of the right ear) plays a similar role in creating this advantage. Does greater exposure to music increase conscious control of cochlear gain and inhibition? Further research is needed to explore the apparent ability of music to promote an enhanced capability of speech in noise recognition.

Bilateral digital hearing aids do not preserve localization cues (see, for example, Van den Bogaert et al., 2006) This means that audiologists when fitting hearing aids to patients (with a mild to moderate age related loss) risk negatively impacting their spatial hearing capability. With those patients who feel that their lack of understanding of speech in background noise is their primary hearing difficulty then hearing aids may simply make their problem even worse - their spatial hearing gain will be reduced by in the region of 10 dB. Although further research is needed, there is a growing number of studies which have shown that open-fit hearing aids are better able to preserve localisation cues (see, for example, Alworth 2011)

Alternatively, the disruption could occur during the process of re-externalizing one's inner voice, resulting in an apparent second voice that seems alien to the individual; a problem that would be interpreted as a level four to level one error.

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."

Sensory processing disorder since 1994 is accepted in the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (DC:0-3R) and is not recognized as a mental disorder in medical manuals such as the ICD-10 or the DSM-5.

Diagnosis is primarily arrived at by the use of standardized tests, standardized questionnaires, expert observational scales, and free play observation at an occupational therapy gym. Observation of functional activities might be carried at school and home as well. Some scales that are not exclusively used in SPD evaluations are used to measure visual perception, function, neurology and motor skills.

Depending on the country, diagnosis is made by different professionals, such as occupational therapists, psychologists, learning specialists, physiotherapists and/or speech and language therapists. In some countries it is recommended to have a full psychological and neurological evaluation if symptoms are too severe.

This may include a blood or other sera test for inflammatory markers such as those for autoinflammatory diseases.

Spatial hearing loss, refers to a form of deafness that is an inability to use spatial cues about where a sound originates from in space. This in turn affects the ability to understand speech in the presence of background noise.

In 73 individual cases reviewed by Evers and Ellger, 57 patients heard tunes that were familiar, while 5 heard unfamiliar tunes. These tunes ranged from religious pieces to childhood favorites, and also included popular songs from the radio. Vocal and instrumental forms of classical music were also identified in some patients. Keshavan found that the consistent feature of musical hallucinations was that it represented a personal memory trace. Memory traces refer to anything that may seem familiar to the patient, which indicated why certain childhood or familiar songs were heard.

As part of differential diagnosis, an MRI scan may be done to check for vascular anomalies, tumors, and structural problems like enlarged mastoids. MRI and other types of scan cannot directly detect or measure age-related hearing loss.