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.

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

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 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."

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.

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.

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.

Dysarthrias are classified in multiple ways based on the presentation of symptoms. Specific dysarthrias include spastic (resulting from bilateral damage to the upper motor neuron), flaccid (resulting from bilateral or unilateral damage to the lower motor neuron), ataxic (resulting from damage to cerebellum), unilateral upper motor neuron (presenting milder symptoms than bilateral UMN damage), hyperkinetic and hypokinetic (resulting from damage to parts of the basal ganglia, such as in Huntington's disease or Parkinsonism), and the mixed dysarthrias (where symptoms of more than one type of dysarthria are present). The majority of dysarthric patients are diagnosed as having 'mixed' dysarthria, as neural damage resulting in dysarthria is rarely contained to one part of the nervous system — for example, multiple strokes, traumatic brain injury, and some kinds of degenerative illnesses (such as amyotrophic lateral sclerosis) usually damage many different sectors of the nervous system.

Ataxic dysarthria is an acquired neurological and sensorimotor speech deficit. It is a common diagnosis among the clinical spectrum of ataxic disorders. Since regulation of skilled movements is a primary function of the cerebellum, damage to the superior cerebellum and the superior cerebellar peduncle is believed to produce this form of dysarthria in ataxic patients. Growing evidence supports the likelihood of cerebellar involvement specifically affecting speech motor programming and execution pathways, producing the characteristic features associated with ataxic dysarthria. This link to speech motor control can explain the abnormalities in articulation and prosody, which are hallmarks of this disorder. Some of the most consistent abnormalities observed in patients with ataxia dysarthria are alterations of the normal timing pattern, with prolongation of certain segments and a tendency to equalize the duration of syllables when speaking. As the severity of the dysarthria increases, the patient may also lengthen more segments as well as increase the degree of lengthening of each individual segment.

Common clinical features of ataxic dysarthria include abnormalities in speech modulation, rate of speech, explosive or scanning speech, slurred speech, irregular stress patterns, and vocalic and consonantal misarticulations.

Ataxic dysarthria is associated with damage to the left cerebellar hemisphere in right-handed patients.

Dysarthria may affect a single system; however, it is more commonly reflected in multiple motor-speech systems. The etiology, degree of neuropathy, existence of co-morbidities, and the individual's response all play a role in the effect the disorder has on the individual's quality of life. Severity ranges from occasional articulation difficulties to verbal speech that is completely unintelligible.

Individuals with dysarthria may experience challenges in the following:

- Timing

- Vocal quality

- Pitch

- Volume

- Breath control

- Speed

- Strength

- Steadiness

- Range

- Tone

Examples of specific observations include a continuous breathy voice, irregular breakdown of articulation, monopitch, distorted vowels, word flow without pauses, and hypernasality.

The exact cause of palilalia is unknown.

Palilalia also occurs in a variety of neurodegenerative disorders, occurring most commonly in Tourette syndrome, Alzheimer's disease, and progressive supranuclear palsy. Such degradation can occur in the substantia nigra where decreased dopamine production results in a loss of function. It can also occur in a variety of genetic disorders including Fragile X syndrome, Prader-Willi syndrome, Asperger's syndrome, autism, and the speaker has no difficulty initiating speech.

Developmental verbal dyspraxia (DVD), also known as childhood apraxia of speech (CAS) and developmental apraxia of speech (DAS), is when children have problems saying sounds, syllables, and words. This is not because of muscle weakness or paralysis. The brain has problems planning to move the body parts (e.g., lips, jaw, tongue) needed for speech. The child knows what they want to say, but their brain has difficulty coordinating the muscle movements necessary to say those words. The exact cause of this disorder is unknown. Some observations suggest a genetic cause of DVD, as many with the disorder have a family history of communication disorders. There is no cure for DVD, but with appropriate, intensive intervention, people with this motor speech disorder can improve significantly.

Motor speech disorders are a class of speech disorders that disturb the body's natural ability to speak due to neurologic impairments. These neurologic impairments make it difficult for individuals with motor speech disorders to plan, program, control, coordinate, and execute speech productions. Disturbances to the individual's natural ability to speak vary in their etiology based on the integrity and integration of cognitive, neuromuscular, and musculoskeletal activities. Speaking is an act dependent on thought and timed execution of airflow and oral motor / oral placement of the lips, tongue, and jaw that can be disrupted by weakness in oral musculature (dysarthria) or an inability to execute the motor movements needed for specific speech sound production (apraxia of speech or developmental verbal dyspraxia). Such deficits can be related to pathology of the nervous system (central and /or peripheral systems involved in motor planning) that affect the timing of respiration, phonation, prosody, and articulation in isolation or in conjunction.

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.

Scanning speech, also known as explosive speech, is a type of ataxic dysarthria in which spoken words are broken up into separate syllables, often separated by a noticeable pause, and spoken with varying force. The sentence "Walking is good exercise", for example, might be pronounced as "Walk (pause) ing is good ex (pause) er (pause) cise". Additionally, stress may be placed on unusual syllables.

The name is derived from literary scansion, because the speech pattern separates the syllables in a phrase much like scanning a poem counts the syllables in a line of poetry.

There is no universal agreement about the exact definition of this term. Some sources require only a noticeable pause between syllables, while others require other speech abnormalities, such as the unusual stress pattern on syllables. Some sources consider it a common, but not necessary, feature of ataxic dysarthria; others consider it exactly synonymous with ataxic dysarthria.

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.

Scanning speech, like other ataxic dysarthrias, is a symptom of lesions in the cerebellum. It is a typical symptom of multiple sclerosis, and it constitutes one of the three symptoms of Charcot's neurologic triad.

Scanning speech may be accompanied by other symptoms of cerebellar damage, such as gait, truncal and limb ataxia, intention tremor, inaccuracies in rapidly repeated movements and sudden, abrupt nausea and vomiting. The handwriting of such patients may also be abnormally large.

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.

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.

Strokes are one of the most common causes of Foix-Chavany-Marie Syndrome. The type of strokes associated with this syndrome include embolic and thrombotic strokes. Strokes affecting the middle cerebral artery and the branches that pass through or near the operculum are characteristic of FCMS.

Symptoms of infections specifically HIV and Herpes simplex encephalitis can cause FCMS. Numerous lesions can develop with HIV infections, which likely result in the development of FCMS.

Dysprosody is usually attributed to neurological damage, such as brain tumors, brain trauma, brain vascular damage, stroke and severe head injury. To better understand the causes of the disease, 25 cases of dysprosody diagnosed between 1907-1978 were examined more closely. It was found that the majority developed dysprosody after a cerebrovascular accident, while another 6 cases developed after a head trauma. In that same study, 16 of the patients were female, while 9 were male. However, there has been no conclusive evidence that gender affects the onset of dysprosody. There has been no evidence that ethnicity, age, or genetics has any impact on the development of dysprosody.

In another reported case in 2004, a patient presented with dysprosody under interesting circumstances. The patient underwent surgery to correct a Reinke's edema, which originates in the vocal folds of the larynx. After the surgery, however, she began speaking in a foreign German accent. Neurological examinations were carried out on the patient through magnetic resonance imaging, but the results were completely normal. The only conclusion the doctors could make was that the surgery somehow changed the patient's vocal identification causing the new voice pattern. It was possible that the patient suffered a lack of oxygen to the brain during the surgery, which would have gone undetected by the resonance imaging, causing dysprosody. Although most causes of dysprosody are due to neurological damage, this case study shows that there can be other causes which are not necessarily neurologically based.

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)

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)

Those who are physically mute may have problems with the parts of the human body required for human speech (the esophagus, vocal cords, lungs, mouth, or tongue, etc.).

Trauma or injury to Broca's area, located in the left inferior frontal cortex of the brain, can cause muteness.

Palilalia (from the Greek πάλιν ("pálin") meaning "again" and λαλιά ("laliá") meaning "speech" or "to talk"), a complex tic, is a language disorder characterized by the involuntary repetition of syllables, words, or phrases. It has features resembling other complex tics such as echolalia or coprolalia, but, unlike other aphasias, palilalia is based upon contextually correct speech.

It was originally described by Alexandre-Achille Souques in a patient with stroke that resulted in left-side hemiplegia, although a condition described as auto-echolalia in 1899 by Édouard Brissaud may have been the same condition.

Pressured speech may also lead to the development of a stutter. The person's need or pressure to speak causes them to involuntarily stutter. Therefore, the person's need to express themselves is greater than their ability to vocalise their thoughts.