In most cases the cause is unknown. However, there are various known causes of speech impediments, such as "hearing loss, neurological disorders, brain injury, intellectual disability, drug abuse, physical impairments such as cleft lip and palate, and vocal abuse or misuse."

Stroke-associated AOS is the most common form of acquired AOS, making up about 60% of all reported acquired AOS cases. This is one of the several possible disorders that can result from a stroke, but only about 11% of stroke cases involve this disorder. Brain damage to the neural connections, and especially the neural synapses, during the stroke can lead to acquired AOS. Most cases of stroke-associated AOS are minor, but in the most severe cases, all linguistic motor function can be lost and must be relearned. Since most with this form of AOS are at least fifty years old, few fully recover to their previous level of ability to produce speech.

Other disorders and injuries of the brain that can lead to AOS include (traumatic) dementia, progressive neurological disorders, and traumatic brain injury.

It is generally accepted that DLD is strongly influenced by genetic factors. The best evidence comes from the Twin study method. Two twins growing up together are exposed to the same home environment, yet may differ radically in their language skills. Such different outcomes are, however, much more common in fraternal (non-identical) twins, who are genetically different. Identical twins share the same genes and tend to be much more similar in language ability. There can be some variation in the severity and persistence of DLD in identical twins, indicating that non-genetic factors affect the course of disorder, but it is unusual to find a child with DLD who has an identical twin with typical language.

There was considerable excitement when a large, multigenerational family with a high rate of DLD were found to have a mutation of the FOXP2 gene just in the affected family members. However, subsequent studies have found that, though DLD runs in families, it is not usually caused by a mutation in FOXP2 or another specific gene. Current evidence suggests that there are many different genes that can influence language learning, and DLD results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. Nevertheless, study of the mode of action of the FOXP2 gene has helped identify other common genetic variants involved in the same neural pathways that may play a part in causing DLD.

Language disorders are associated with aspects of home environment, and it is often assumed that this is a causal link, with poor language stimulation leading to weak language skills. Twin studies, however, show that two children in the same home environment can have very different language outcomes, suggesting we should consider other explanations for the link. Children with DLD often grow up into adults who have relatively low educational attainments, and their children may share a genetic risk for language disorder.

One non-genetic factor that is known to have a specific impact on language development is being a younger sibling in a large family.

Specific language impairment (SLI) is diagnosed when a child has delayed or disordered language development for no apparent reason. Usually the first indication of SLI is that the child is later than usual in starting to speak and subsequently is delayed in putting words together to form sentences. Spoken language may be immature. In many children with SLI, understanding of language, or "receptive" language, is also impaired, though this may not be obvious unless the child is given a formal assessment.

Although difficulties with use and understanding of complex sentences are a common feature of SLI, the diagnostic criteria encompass a wide range of problems, and for some children other aspects of language are problematic (see below). In general, the term SLI is reserved for children whose language difficulties persist into school age, and so it would not be applied to toddlers who are late to start talking, most of whom catch up with their peer group after a late start.

Longitudinal studies indicate that problems are largely resolved by 5 years of age in around 40% of 4-year-olds with early language delays who have no other presenting risk factors. However, for children who still have significant language difficulties at school entry, reading problems are common, even for children who receive specialist help, and educational attainments are typically poor. Poor outcomes are most common in cases where comprehension as well as expressive language is affected. There is also evidence that scores on tests of nonverbal ability of children with DLD decrease over the course of development.

DLD is associated with an elevated risk of social, emotional and mental health concerns. For instance, in a UK survey, 64% of a sample of 11-year-olds with DLD scored above a clinical threshold on a questionnaire for psychiatric difficulties, and 36% were regularly bullied, compared with 12% of comparison children. In the longer-term, studies of adult outcomes of children with DLD have found elevated rates of unemployment, social isolation and psychiatric disorder among those with early comprehension difficulties. However, better outcomes are found for children who have milder difficulties and do not require special educational provision.

DVD/CAS is a motor disorder, which means that the problem is located in the brain and its signals, and not in the mouth. In most cases, the cause is unknown. Possible causes include genetic syndromes and disorders.

Recent research has focused on the significance of the FOXP2 gene in both species and individual development.

Research regarding the KE family, where half the members of the extended family, over three generations, exhibited heritable developmental verbal dyspraxia, were found to have a defective copy of the FOXP2 gene. and further studies suggest that the FOXP2 gene as well as other genetic issues could explain DVD/CAS. including 16p11.2 microdeletion syndrome.

Birth/prenatal injuries, as well as stroke, can also be causes of DVD/CAS. Furthermore, DVD/CAS can occur as a secondary characteristic to a variety of other conditions. These include autism, some forms of epilepsy, fragile X syndrome, galactosemia, and chromosome translocations involving duplications or deletions.

Specific language impairment (SLI) is diagnosed when a child's language does not develop normally and the difficulties cannot be accounted for by generally slow development, physical abnormality of the speech apparatus, autism spectrum disorder, apraxia, acquired brain damage or hearing loss. Twin studies have shown that it is under genetic

influence. Although language impairment can result from a single-gene mutation, this is unusual. More commonly SLI results from the combined influence of multiple genetic variants, each of which is found in the general population, as well as environmental influences.

Language delays are the most frequent developmental delays, and can occur for many reasons. A delay can be due to being a “late bloomer,” or a more serious problem. The most common causes of speech delay include

- Hearing loss

- Slow development

- Intellectual Disability

Such delays can occur in conjunction with a lack of mirroring of facial responses, unresponsiveness or unawareness of certain noises, a lack of interest in playing with other children or toys, or no pain response to stimuli.

Other causes include:

- Psychosocial deprivation - The child doesn't spend enough time talking with adults. Research on early brain development shows that babies and toddlers have a critical need for direct interactions with parents and other significant care givers for healthy brain growth and the development of appropriate social, emotional, and cognitive skills.

- Television viewing is associated with delayed language development. Children who watched television alone were 8.47 times more likely to have language delay when compared to children who interacted with their caregivers during television viewing. As recommended by the American Academy of Pediatrics (AAP), children under the age of 2 should watch no television at all, and after age 2 watch no more than one to two hours of quality programming a day. Therefore, exposing such young children to television programs should be discouraged. Parents should engage children in more conversational activities to avoid television-related delays to their children language development, which could impair their intellectual performance.

- Stress during pregnancy is associated with language delay.

- Being a twin

- Attention deficit hyperactivity disorder

- Autism (a developmental disorder) - There is strong evidence that autism is commonly associated with language delay. Asperger syndrome, which is on the autistic spectrum, however, is not associated with language delay.

- Selective mutism (the child just doesn't want to talk)

- Cerebral palsy (a movement disorder caused by brain damage)

- Genetic abnormalities - In 2005, researchers found a connection between expressive language delay and a genetic abnormality: a duplicate set of the same genes that are missing in sufferers of Williams-Beuren syndrome. Also so called XYY syndrome can often cause speech delay.

- Correlation with male sex, previous family history, and maternal education has been demonstrated.

Recent research has established the existence of primary progressive apraxia of speech caused by neuroanatomic motor atrophy. For a long time, this disorder was not distinguished from other motor speech disorders such as dysarthria and in particular primary progressive aphasia. Many studies have been done trying to identify areas in the brain in which this particular disorder occurs or at least to show that it occurs in different areas of the brain than other disorders. One study observed 37 patients with neurodegenerative speech disorders to determine whether or not it is distinguishable from other disorders, and if so where in the brain it can be found. Using speech and language, neurological, neuropsychological and neuroimaging testing, the researchers came to the conclusion that PAS does exist and that it correlates to superior lateral premotor and supplementary motor atrophy. However, because PAS is such a rare and recently discovered disorder, many studies do not have enough subjects to observe to make data entirely conclusive.

In 2006, the U.S. Department of Education indicated that more than 1.4 million students were served in the public schools' special education programs under the speech or language impairment category of IDEA 2004. This estimate does not include children who have speech/language problems secondary to other conditions such as deafness; this means that if all cases of speech or language impairments were included in the estimates, this category of impairment would be the largest. Another source has estimated that communication disorders—a larger category, which also includes hearing disorders—affect one of every 10 people in the United States.

ASHA has cited that 24.1% of children in school in the fall of 2003 received services for speech or language disorders—this amounts to a total of 1,460,583 children between 3 –21 years of age. Again, this estimate does not include children who have speech/language problems secondary to other conditions. Additional ASHA prevalence figures have suggested the following:

- Stuttering affects approximately 4% to 5% of children between the ages of 2 and 4.

- ASHA has indicated that in 2006:

- Almost 69% of SLPs served individuals with fluency problems.

- Almost 29% of SLPs served individuals with voice or resonance disorders.

- Approximately 61% of speech-language pathologists in schools indicated that they served individuals with SLI

- Almost 91% of SLPs in schools indicated that they servedindividuals with phonological/articulation disorder

- Estimates for language difficulty in preschool children range from 2% to 19%.

- Specific Language Impairment (SLI) is extremely common in children, and affects about 7% of the childhood population.

Studies have failed to find clear evidence that language delay can be prevented by training or educating health care professionals in the subject. Overall, some of the reviews show positive results regarding interventions in language delay, but are not curative. (Commentary - Early Identification of Language Delays, 2005)

There are three significant features that differentiate DVD/CAS from other childhood speech sound disorders. These features are:

- "Inconsistent errors on consonants and vowels in repeated productions of syllables and words

- Lengthened coarticulatory transitions between sounds and syllables

- Inappropriate prosody, especially in the realization of lexical or phrasal stress"

Even though DVD/CAS is a "developmental" disorder, it will not simply disappear when children grow older. Children with this disorder do not follow typical patterns of language acquisition and will need treatment in order to make progress.

Dysprosody, which may manifest as pseudo-foreign accent syndrome, refers to a disorder in which one or more of the prosodic functions are either compromised or eliminated completely.

Prosody refers to the variations in melody, intonation, pauses, stresses, intensity, vocal quality, and accents of speech. As a result, prosody has a wide array of functions, including expression on linguistic, attitudinal, pragmatic, affective and personal levels of speech. People diagnosed with dysprosody most commonly experience difficulties in pitch or timing control. Essentially, people diagnosed with the disease can comprehend language and vocalize what they intend to say, however, they are not able to control the way in which the words come out of their mouths. Since dysprosody is the rarest neurological speech disorder discovered, not much is conclusively known or understood about the disorder. The most obvious expression of dysprosody is when a person starts speaking in an accent which is not their own. Speaking in a foreign accent is only one type of dysprosody, as the disease can also manifest itself in other ways, such as changes in pitch, volume, and rhythm of speech. It is still very unclear as to how damage to the brain causes the disruption of prosodic function. The only form of effective treatment developed for dysprosody is speech therapy.

Speech disorders or speech impediments are a type of communication disorder where 'normal' speech is disrupted. This can mean stuttering, lisps, etc. Someone who is unable to speak due to a speech disorder is considered mute.

A speech sound disorder is a speech disorder in which some speech sounds (called phonemes) in a child's (or, sometimes, an adult's) language are either not produced, not produced correctly, or are not used correctly. The term protracted phonological development is sometimes preferred when describing children's speech to emphasize the continuing development while acknowledging the delay.

Most speech sound disorders occur without a known cause. A child may not learn how to produce sounds correctly or may not learn the rules of speech sounds on his or her own. These children may have a problem with speech development, which does not always mean that they will simply outgrow it by themselves. Many children do develop speech sounds over time but those who do not often need the services of a Speech-Language Pathologist to learn correct speech sounds.

Some speech sound errors can result from other syndromes or disorders such as:

- developmental disorders (e.g. autism)

- genetic disorders (e.g. Down syndrome)

- hearing loss, including temporary hearing loss, such as from ear infections

- cleft palate or other physical anomalies of the mouth

- illness

- neurological disorders (e.g. cerebral palsy)

Expressive language disorder is a communication disorder in which there are difficulties with verbal and written expression. It is a specific language impairment characterized by an ability to use expressive spoken language that is markedly below the appropriate level for the mental age, but with a language comprehension that is within normal limits. There can be problems with vocabulary, producing complex sentences, and remembering words, and there may or may not be abnormalities in articulation.

As well as present speech production, very often, someone will have difficulty remembering things. This memory problem is only disturbing for speech; non-verbal or non-linguistically based memory will be unimpaired. An example of a child with expressive language disorder can be seen here.

Expressive language disorder affects work and schooling in many ways. It is usually treated by specific speech therapy, and usually cannot be expected to go away on its own.

Expressive language disorder can be further classified into two groups: developmental expressive language disorder and acquired expressive language disorder. Developmental expressive language disorder currently has no known cause, is first observed when a child is learning to talk, is more common in boys than girls, and is much more common than the acquired form of the disorder. Acquired expressive language disorder is caused by specific damage to the brain by a stroke, traumatic brain injury, or seizures.

Care must be taken to distinguish expressive language disorder from other communication disorders, sensory-motor disturbances, intellectual disability and/or environmental deprivation (see DSM-IV-TR criterion D). These factors affect a person's speech and writing to certain predictable extents, and with certain differences.

Careful diagnosis is also important because "atypical language development can be a secondary characteristic of other physical and developmental problems that may first manifest as language problems".

Developmental verbal dyspraxia is a developmental inability to motor plan volitional movement for the production of speech in the absence of muscular weakness. Research has suggested links to the FOXP2 gene.

A communication disorder is any disorder that affects an individual's ability to comprehend, detect, or apply language and speech to engage in discourse effectively with others. The delays and disorders can range from simple sound substitution to the inability to understand or use one's native language.

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.

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 many potential causes of dysarthria. They include toxic, metabolic, degenerative diseases, traumatic brain injury, or thrombotic or embolic stroke.

Degenerative diseases include parkinsonism, amyotrophic lateral sclerosis (ALS), multiple sclerosis, Huntington's disease, Niemann-Pick disease, and Friedreich ataxia.

Toxic and metabolic conditions include: Wilson's disease, hypoxic encephalopathy such as in drowning, and central pontine myelinolysis.

These result in lesions to key areas of the brain involved in planning, executing, or regulating motor operations in skeletal muscles (i.e. muscles of the limbs), including muscles of the head and neck (dysfunction of which characterises dysarthria). These can result in dysfunction, or failure of: the motor or somatosensory cortex of the brain, corticobulbar pathways, the cerebellum, basal nuclei (consisting of the putamen, globus pallidus, caudate nucleus, substantia nigra etc.), brainstem (from which the cranial nerves originate), or the neuro-muscular junction (in diseases such as myasthenia gravis) which block the nervous system's ability to activate motor units and effect correct range and strength of movements.

Causes:

- Brain tumor

- Cerebral palsy

- Guillain–Barré syndrome

- Hypothermia

- Lyme disease

- Stroke

- Intracranial hypertension (formerly known as pseudotumor cerebri)

- Tay-Sachs, and late onset Tay-Sachs (LOTS), disease

The most common cause of asemia is brain damage, such as a stroke or a brain tumor. Other possible causes include Alzheimer's disease and infection. Roger Wolcott Sperry, through his research of split-brain patients, had found out that the human brain lateralizes functions, meaning that the two hemispheres of the brain have different functions. Brain damage, specifically to the left hemisphere, can impair our ability to speak or understand language. This led Sperry to conclude that due to the lateralization of brain function, language is based in the left hemisphere. Therefore, any kind of brain damage to the left hemisphere will greatly impact language, whether it is expressive or receptive.

Muteness or mutism () is an inability to speak, often caused by a speech disorder, hearing loss, or surgery. Someone who is mute may be so due to the unwillingness to speak in certain social situations.

In relation to other types of aphasia, TMoA occurs less frequently, so there is less information on its prognosis. In general, for individuals with aphasia, most recovery is seen within 6 months of the stroke or injury although more recovery may continue in the following months or years. The timeline of recovery may look different depending on the type of stroke that caused the aphasia. With an ischemic stroke, recovery is greatest within the first two weeks and then diminishes overtime until the progress stabilizes. With a hemorrhagic stroke, the patient often shows little improvement in the first few weeks and then has relatively rapid recovery until they stabilize.

In a study involving eight patients with border zone lesions, all patients presented with transcortical mixed aphasia initially after the stroke. Three of these patients made a complete recovery within a few days post-stroke. For three other patients with more anterior lesions, their aphasia transitioned to TMoA. All participants in the study regained full language abilities within 18 months following their stroke. This suggests a positive long-term prognosis for patients with TMoA. However, this might not be the case for all patients and more research is needed in order to solidify these findings. Another study found that prognosis of TMoA is affected by lesion size. Smaller lesions typically cause delays in speech initiation; whereas, larger lesions lead to more profound language abnormalities and difficulty with abstract language abilities.

Research has shown that treatment has a direct effect on aphasia outcomes. Intensity, duration and timing of treatment all need to be taken in to consideration when choosing a course of treatment and determining a prognosis. In general, greater intensity leads to greater improvement. For duration, longer-term treatment produces more permanent changes. As for timing, beginning treatment too early may be difficult for the system which has not recovered enough to do intensive therapy, but beginning too late may result missing the window of the opportunity in which the most change can occur. Neuroplasticity, the brain's natural ability to reorganize itself following a traumatic event, occurs best when treatment connects simultaneous events, maintains attention, taps into positive emotion, utilizes repetition tasks, and is specific to the individual's needs.

Other factors affecting prognosis includes location and site of lesion. Since the lesion that results in TMoA usually occurs in the watershed area and does not directly involve the areas of the brain responsible for general language abilities, prognosis for these patients is good overall. Other factors that determine a patient’s prognosis include age, education prior to the stroke, gender, motivation, and support.