Neuroscientists have learned a lot about the role of the brain in numerous cognitive mechanisms by understanding corresponding disorders. Similarly, neuroscientists have come to learn a lot about music cognition by studying music-specific disorders. Even though music is most often viewed from a "historical perspective rather than a biological one" music has significantly gained the attention of neuroscientists all around the world. For many centuries music has been strongly associated with art and culture. The reason for this increased interest in music is because it "provides a tool to study numerous aspects of neuroscience, from motor skill learning to emotion".

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.

Hypoacusis is defined as impairment in hearing or deafness. Hypoacusis is one of five etiologies of musical hallucinations, and is the most common in the case studies reviewed by Evers and Ellgers. According to Sanchez et al. 2011, there have been suggestions that pontine lesions could alter the central auditory system's function causing hypoacusis and musical hallucinations.

Investigators have successfully narrowed down the major factors that are associated with musical hallucinations. Evers and Ellgers compiled a significant portion of musical hallucination articles, case studies etc. and were able to categorize five major etiologies:

- Hypoacusis

- Psychiatric disorders

- Focal brain lesion

- Epilepsy

- Intoxication

Developmental coordination disorder is a lifelong neurological condition that is more common in males than in females, with a ratio of approximately four males to every female. The exact proportion of people with the disorder is unknown since the disorder can be difficult to detect due to a lack of specific laboratory tests, thus making diagnosis of the condition one of elimination of all other possible causes/diseases. Approximately 5–6% of children are affected by this condition.

Auditory verbal agnosia (AVA), also known as pure word deafness, is the inability to comprehend speech. Individuals with this disorder lose the ability to understand language, repeat words, and write from dictation. Some patients with AVA describe hearing spoken language as meaningless noise, often as though the person speaking was doing so in a foreign language. However, spontaneous speaking, reading, and writing are preserved. The maintenance of the ability to process non-speech auditory information, including music, also remains relatively more intact than spoken language comprehension. Individuals who exhibit pure word deafness are also still able to recognize non-verbal sounds. The ability to interpret language via lip reading, hand gestures, and context clues is preserved as well. Sometimes, this agnosia is preceded by cortical deafness; however, this is not always the case. Researchers have documented that in most patients exhibiting auditory verbal agnosia, the discrimination of consonants is more difficult than that of vowels, but as with most neurological disorders, there is variation among patients.

Auditory verbal agnosia (AVA) is not the same as Auditory agnosia; patients with (nonverbal) auditory agnosia have a relatively more intact speech comprehension system despite their impaired recognition of nonspeech sounds.

Auditory verbal agnosia has been shown to form as a result of tumor formation, especially in the posterior third ventricle, trauma, lesions, cerebral infarction, encephalitis as a result of herpes simplex, and Landaui-Kleffner syndrome. The exact location of damage which results in pure word deafness is still under debate, but the planum temporale, posterior STG, and white matter damage to the acoustic radiations (AR) have all been implicated.

Auditory verbal agnosia is rarely diagnosed in its pure form. Auditory verbal agnosia can both present as the result of acute damage or as chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. In contrast, auditory verbal agnosia has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. MRIs showed cortical atrophy in the left superior temporal lobe region.

In childhood, auditory verbal agnosia can also be caused by Landau-Kleffner syndrome, also called acquired epileptic aphasia. It is often the first symptom of this disease. A review of 45 cases suggested a relationship between prognosis and age of onset with poorer prognosis for those with earlier onset. In extremely rare cases, auditory verbal agnosia has been known to present as a symptom of neurodegenerative disease, such as Alzheimer's disease. In such cases auditory verbal agnosia is a symptom that is typically followed by more severe neurological symptoms typical of Alzheimer's disease.

Selective mutism (SM) is an umbrella term for the condition of otherwise well-developed children who cannot speak or communicate under certain settings. The exact causes that affect each child may be different and yet unknown. There have been attempts to categorize, but there are no definitive answers yet due to the under-diagnosis and small/biased sample sizes. Many people are not diagnosed until late in childhood only because they do not speak at school and therefore fail to accomplish assignments requiring public speaking. Their involuntary silence makes the condition harder to understand or test. Parents often are unaware of the condition since the children may be functioning well at home. Teachers and pediatricians also sometimes mistake it for severe shyness or common stage fright.

Selective mutism occurs in all ethnic groups. The majority of reported cases are of white and multiethnic children. However this could be due to under-diagnosis and under-reporting in other ethnic groups.

Most children with selective mutism are hypothesized to have an inherited predisposition to anxiety. They often have inhibited temperaments, which is hypothesized to be the result of over-excitability of the area of the brain called the amygdala. This area receives indications of possible threats and sets off the fight-or-flight response. Given the very high overlap between social anxiety disorder and selective mutism (as high as 100% in some studies), it is possible that social anxiety disorder causes selective mutism.

Some children with selective mutism may have trouble processing sensory information. This would cause anxiety and a sense of being overwhelmed in unfamiliar situations, which may cause the child to "shut down" and not be able to speak (something that some autistic people also experience). Many children with selective mutism have some auditory processing difficulties.

About 20–30% of children with SM have speech or language disorders that add stress to situations in which the child is expected to speak.

Despite the change of name from "elective" to "selective", a common misconception remains that a selectively mute child is defiant or stubborn. In fact, children with SM have a lower rate of oppositional behavior than their peers in a school setting. Some previous studies on the subject of selective mutism have been dismissed as containing serious flaws in their design. According to a more recent systematic study it is believed that children who have selective mutism are not more likely than other children to have a history of early trauma or stressful life events. Another recent study by Dummit et al., in 1997 did not find any evidence of trauma in their sample of children. Recent evidence has shown that trauma does not explain why most children with selective mutism develop the condition. Many children who have selective mutism almost always speak confidently in some situations. Children who have experienced trauma however are known to suddenly stop speaking.

Auditory arrhythmia is the inability to rhythmically perform music, to keep time, and to replicate musical or rhythmic patterns. It has been caused by damage to the cerebrum or rewiring of the brain.

Apperceptive agnosia is a failure in recognition that is due to a failure of perception. In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur. When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; This occurs because apperceptive agnosia is most likely to present visual impairments. However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas.

Semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain (with loss of word meaning). SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD), with the other two being frontotemporal dementia and progressive nonfluent aphasia. SD is a clinically defined syndrome, but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). SD is one of the three variants of Primary Progressive Aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease. It is important to note the distinctions between Alzheimer’s Disease and Semantic dementia with regard to types of memory affected. In general, Alzheimer’s Disease is referred to as disorder affecting mainly episodic memory, defined as the memory related to specific, personal events distinct for each individual. Semantic dementia generally affects semantic memory, which refers to long-term memory that deals with common knowledge and facts.3

It was first described by Arnold Pick in 1904 and in modern times was characterized by Professor Elizabeth Warrington in 1975, but it was not given the name semantic dementia until 1989. The clinical and neuropsychological features, and their association with temporal lobe atrophy were described by Professor John Hodges and colleagues in 1992.

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

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

At times, speech delay and impairment is caused by a physical disruption in the mouth such as a deformed frenulum, lips, or palate. If the motion or ability to form words and appropriate sounds is disrupted, the child may be slow to pick up words and lack the ability to shape their mouth and tongue in the formation of words.

Other more serious concerns are those that can be caused by oral-motor issues. Oral-motor dysfunction refers to a lack or delay in the area of the brain that speech is formed and created and communicated to the mouth and tongue. While speech may be the only concern, this disorder can be highlighted with feeding issues as well.

Children that are having speech delay disorders could have the following characteristics (Shriberg 1982):

- Speech mechanism in which speech is associated with hearing, motor speech and craniofacial malfunction

- Cognitive-linguistic aspects in which the impairment is associated with the child's intellectual, receptive, expressive and linguistic ability.

- Psychosocial issues in which the impairment is associated with caregiver, school environment, and the child's self behaviors such as aggression and maturity

The many other causes of speech delay include bilingual children with phonological disorders autism spectrum disorders, childhood apraxia, Auditory processing disorder, prematurity, cognitive impairment and hearing loss. Broomfield and Dodd's (2004a) found out after survey that 6.4% of children who are perfectly normal showed speech difficulty while they lacked these disorders will often show early signs and are at times identified as "at risk" when the speech delay is diagnosed.

There are a range of music-specific disorders that afflict many individuals in any given population. However, since music cognition is a newly developing area of interest in the neuroscientific community, a lot more research is yet to be done and the knowledge that currently exists is vague and indefinitive. The inability to recognize or reproduce music is a major psychological disorder, as it incapacitates an individual to appreciate music and experience its therapeutic powers. Music is known for its healing and relaxing properties, therefore it is even more important that more robust experiments and research be performed in this relatively new area of neuroscience.

There is currently no known curative treatment for SD. The average duration of illness is 8–10 years, and its progression cannot be slowed. Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible.

Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.

SD has no known preventative measures.

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.

Contrary to popular belief, people with selective mutism do not necessarily improve with age. Effective treatment is necessary for a child to develop properly. Without treatment, selective mutism can contribute to chronic depression, further anxiety, and other social and emotional problems.

Consequently, treatment at an early age is important. If not addressed, selective mutism tends to be self-reinforcing. Others may eventually expect an afflicted child to not speak and therefore stop attempting to initiate verbal contact. Alternatively, they may pressure the child to talk, increasing their anxiety levels in situations where speech is expected. Due to these problems, a change of environment may be a viable consideration. However, changing school is worth considering only if the alternative environment is highly supportive, otherwise a whole new environment could also be a social shock for the individual and/or deprive them of any friends or support they have currently. Regardless of the cause, increasing awareness and ensuring an accommodating, supportive environment are the first steps towards effective treatment. Most often afflicted children do not have to change schools or classes and have no difficulty keeping up except on the communication and social front. Treatment in teenage or adult years can be more difficult because the afflicted individual has become accustomed to being mute.

The exact treatment depends on the person's age, any comorbid mental illnesses, and a number of other factors. For instance, stimulus fading is typically used with younger children because older children and teenagers recognize the situation as an attempt to make them speak, and older people with this condition and people with depression are more likely to need medication.

Like other disabilities, adequate accommodations are needed for the afflicted to succeed at school, work, and in the home. Under the U.S. federal law and the Individuals with Disabilities Education Act (IDEA), those with the disorder qualify for services based upon the fact that they have an impairment that hinders their ability to speak, thus disrupting their lives. This assistance is typically documented in the form of an Individual Educational Plan (IEP). Post-secondary accommodations are also available for people with disabilities.

Under another law, Section 504 of the Rehabilitation Act of 1973, public school districts are required to provide a free, appropriate public education to every "qualified handicapped person" residing within their jurisdiction. If the child is found to have impairments that substantially limit a major life activity (in this case, learning), the education agency has to decide what related aids or services are required to provide equal access to the learning environment.

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.

An individual with this condition has an especially difficult time maintaining a steady beat, and even has difficulty following along to a steady rhythm. Before it was a known disorder, it was thought that these individuals were just severely uncoordinated, and therefore were unable to follow along with the music. It has been discovered recently that problems with rhythm in Schizophrenia, Parkinson's, and Attention Deficit Hyperactive Disorder are also found to have a correlation to rhythm deficiencies.

Speech delay, also known as alalia, refers to a delay in the development or use of the mechanisms that produce speech. Speech, as distinct from language, refers to the actual process of making sounds, using such organs and structures as the lungs, vocal cords, mouth, tongue, teeth, etc. Language delay refers to a delay in the development or use of the knowledge of language.

Because language and speech are two independent stages, they may be individually delayed. For example, a child may be delayed in speech (i.e., unable to produce intelligible speech sounds), but not delayed in language. In this case, the child would be attempting to produce an age appropriate amount of language, but that language would be difficult or impossible to understand. Conversely, since a child with a language delay typically has not yet had the opportunity to produce speech sounds, it is likely to have a delay in speech as well.

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.

The occurrence of MES has been suggested to be very high among the hearing impaired through acquired deafness or the ear condition known as tinnitus. Though exact causation is uncertain, it has been theorized that the "release phenomenon" is taken into effect. The "release phenomenon" says that individuals with acquired deafness may experience musical hallucinations because the lack of stimulation, which can give room for the brain to interpret internal sounds as being external.

Sufferers typically hear music or singing and the condition is more common in women. The hallucinatory experiences differ from that commonly experienced in psychotic disorders although there may be some overlap. The most important distinction is the realization that the hallucinations are not real. Delusional beliefs associated with the hallucinations may occur, but some degree of insight should be preserved. There should not be any other psychotic symptoms present, especially hallucinations in other modalities.

Amusia is a musical disorder that appears mainly as a defect in processing pitch but also encompasses musical memory and recognition. Two main classifications of amusia exist: acquired amusia, which occurs as a result of brain damage, and congenital amusia, which results from a music-processing anomaly present since birth.

Studies have shown that congenital amusia is a deficit in fine-grained pitch discrimination and that 4% of the population suffers from this disorder. Acquired amusia, on the other hand, may take several forms. Patients with brain damage may experience the loss of ability to produce musical sounds while sparing speech, much like aphasics lose speech selectively but can sometimes still sing. Other forms of amusia may affect specific sub-processes of music processing. Current research has demonstrated dissociations between rhythm, melody, and emotional processing of music, and amusia may include impairment of any combination of these skill sets.