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 verbal agnosia can be referred to as a pure aphasia because it has a high degree of specificity. Despite an inability to comprehend speech, patients with auditory verbal agnosia typically retain the ability to hear and process non-speech auditory information, speak, read and write. This specificity suggests that there is a separation between speech perception, non-speech auditory processing, and central language processing. In support of this theory, there are cases in which speech and non-speech processing impairments have responded differentially to treatment. For example, some therapies have improved writing comprehension in patients over time, while speech remained critically impaired in those same patients.

The term "pure word deafness" is something of a misnomer. By definition, individuals with pure word deafness are not deaf – in the absence of other impairments, these individuals have normal hearing for all sounds, including speech. The term "deafness" originates from the fact that individuals with AVA are unable to "comprehend" speech that they hear. The term "pure word" refers to the fact that comprehension of verbal information is selectively impaired in AVA. For this reason, AVA is distinct from other auditory agnosias in which the recognition of nonspeech sounds is impaired. Classical (or pure) auditory agnosia is an inability to process environmental sounds. Interpretive or receptive agnosia (amusia) is an inability to understand music.

Patients with pure word deafness complain that speech sounds simply do not register, or that they tend not to come up. Other claims include speech sounding as if it were in a foreign language, the words having a tendency to run together, or the feeling that speech was simply not connected to the patient's voice.

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.

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.

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.

Amusia may be congenital or acquired. Congenital amusia, as the term suggests, is acquired as a result of birth or one's genes; while acquired amusia occurs as a result of accidental brain damage, stress, or cognitive deficits. Symptoms of this disease vary from lack of basic melodic discrimination, recognition despite normal audiometry, above average intellectual, memory, as well as language skills (Peretz 2002). Another conspicuous symptom of amusia is the ability of the affected individual to carry out normal speech, however, he or she is unable to sing. Amusic individuals "show a particular deficit in discriminating musical pitch variations and in recognizing familiar melodies". Neuroscientists are now classifying congenital amusia as a "new class of learning disabilities that affect musical abilities" (Ayotte 2002).

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.

There are two general classifications of amusia: congenital amusia and acquired amusia.

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

Besides lack of speech, other common behaviors and characteristics displayed by selectively mute people, according to Dr. Elisa Shipon-Blum's findings, include:

- Shyness, social anxiety, fear of social embarrassment, and/or social isolation and withdrawal

- Difficulty maintaining eye contact

- Blank expression and reluctance to smile

- Difficulty expressing feelings, even to family members

- Tendency to worry more than most people of the same age

- Sensitivity to noise and crowds

On the positive side, many people with this condition have:

- Above-average intelligence, perception, or inquisitiveness

- Creativity and a love for art or music

- Empathy and sensitivity to others' thoughts and feelings

- A strong sense of right and wrong

The warning signs of early speech delay are categorized into age related milestones, beginning at the age of 12 months and continuing through early adolescence.

At the age of 12 months, there is cause for concern if the child is not able to do the following:

- Using gestures such as waving good-bye and pointing at objects

- Practicing the use of several different consonant sounds

- Vocalizing or communicating needs

Between the ages of 15 and 18 months children are at a higher risk for speech delay if they are displaying the following:

- Not saying "momma" and "dada"

- Not reciprocating when told "no", "hello", and "bye"

- Does not have a one to three word vocabulary at 12 months and up to 15 words by 18 months

- Is unable to identify body parts

- Displaying difficulties imitating sounds and actions

- Shows preference to gestures over verbalization

Additional signs of speech delay after the age of 2 years and up to the age of 4 include the following:

- Inability to spontaneously produce words and phrases

- Inability to follow simple directions and commands

- Cannot make two word connections

- Lacks consonant sounds at the beginning or end of words

- Is difficult to understand by close family members

- Is not able to display the tasks of common household objects

- Is unable to form simple 2 to 3 word sentences

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.

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.

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.

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.

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.

Children and adults with selective mutism are fully capable of speech and understanding language but fail to speak in certain situations, though speech is expected of them. The behaviour may be perceived as shyness or rudeness by others. A child with selective mutism may be completely silent at school for years but speak quite freely or even excessively at home. There is a hierarchical variation among people with this disorder: some people participate fully in activities and appear social but do not speak, others will speak only to peers but not to adults, others will speak to adults when asked questions requiring short answers but never to peers, and still others speak to no one and participate in few, if any, activities presented to them. In a severe form known as "progressive mutism", the disorder progresses until the person with this condition no longer speaks to anyone in any situation, even close family members.

Selective mutism is by definition characterized by the following:

- Consistent failure to speak in specific social situations (in which there is an expectation for speaking, e.g., at school) despite speaking in other situations.

- The disturbance interferes with educational or occupational achievement or with social communication.

- The duration of the disturbance is at least 1 month (not limited to the first month of school).

- The failure to speak is not due to a lack of knowledge of, or comfort with, the spoken language required in the social situation.

- The disturbance is not better accounted for by a communication disorder (e.g., childhood-onset fluency disorder) and does not occur exclusively during the course of autism spectrum disorder, schizophrenia, or another psychotic disorder.

Selective mutism is strongly associated with other anxiety disorders, particularly social anxiety disorder. In fact, the majority of children diagnosed with selective mutism also have social anxiety disorder (100% of participants in two studies and 97% in another). Some researchers therefore speculate that selective mutism may be an avoidance strategy used by a subgroup of children with social anxiety disorder to reduce their distress in social situations.

Particularly in young children, SM can sometimes be confused with an autism spectrum disorder, especially if the child acts particularly withdrawn around his or her diagnostician, which can lead to incorrect treatment. Although autistic people may also be selectively mute, they often display other behaviors—hand flapping, repetitive behaviors, social isolation even among family members (not always answering to name, for example)—that set them apart from a child with selective mutism. Some autistic people may be selectively mute due to anxiety in social situations that they do not fully understand. If mutism is entirely due to autism spectrum disorder, it cannot be diagnosed as selective mutism as stated in the last item on the list above.

The former name "elective mutism" indicates a widespread misconception among psychologists that selective mute people choose to be silent in certain situations, while the truth is that they often wish to speak but have difficulty doing so. To reflect the involuntary nature of this disorder, the name was changed to "selective mutism" in 1994.

The incidence of selective mutism is not certain. Due to the poor understanding of this condition by the general public, many cases are likely undiagnosed. Based on the number of reported cases, the figure is commonly estimated to be 1 in 1000, 0.1%. However, a 2002 study in "The Journal of the American Academy of Child and Adolescent Psychiatry" estimated the incidence to be 0.71%.

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

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.

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

The defining characteristic of SD is decreased performance on tasks that require semantic memory. This includes difficulty with naming pictures and objects, single word comprehension, categorizing, and knowing uses and features of objects. SD patients also have difficulty with spontaneous speech creation, using words such as "this" or "things" where more specific and meaningful words can be used. Syntax is spared, and SD patients have the ability to discern syntactic violations and comprehend sentences with minimal lexical demands. SD patients have selectively worse concrete word knowledge and association, but retain knowledge and understanding of abstract words. SD patients are able to retain knowledge of numbers and music, but have more difficulty with concrete concepts with visual associations. Impairments of processing of phonemic structure and prosodic predictability have also been observed.

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.

Sensory dysfunction disorder is a reported neurological disorder of information processing, characterized by difficulty in understanding and responding appropriately to sensory inputs. Sensory dysfunction disorder is not recognized by the American Medical Association. "Sensory processing (SP) difficulties have been reported in as many as 95% of children with autism, however, empirical research examining the existence of specific patterns of SP difficulties within this population is scarce."

The brain receives messages from the body's sensory systems, which informs the brain of what is going on around and to a person's body. If one or more of these systems become overstimulated, it may result in what is known as Sensory Dysfunction Disorder. An example of a response to overstimulation is expressed by A. Jean Ayres, in "Sensory Integration and the Child: Understanding Hidden Sensory Challenges". She writes, "When the flow of sensations is disorganized, life can be like a rush-hour traffic jam” (p. 289). The following sensory systems are broken down into individual categories to better understand the impact a sensitivity can have on an individual.

Developmental verbal dyspraxia (DVD) is a type of ideational dyspraxia, causing speech and language impairments. This is the favoured term in the UK; however, it is also sometimes referred to as articulatory dyspraxia, and in the United States the usual term is childhood apraxia of speech (CAS).

Key problems include:

- Difficulties controlling the speech organs.

- Difficulties making speech sounds

- Difficulty sequencing sounds

- Within a word

- Forming words into sentences

- Difficulty controlling breathing, suppressing salivation and phonation when talking or singing with lyrics.

- Slow language development

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.