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.

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.

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.

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.

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.

Apraxia is most often due to a lesion located in the dominant (usually left) hemisphere of the brain, typically in the frontal and parietal lobes. Lesions may be due to stroke, acquired brain injuries, or neurodegenerative diseases such as Alzheimer's disease or other dementias, Parkinson's disease, or Huntington's disease. It is also possible for apraxia to be caused by lesions in other areas of the brain including the non-dominant (usually right) hemisphere.

Ideomotor apraxia is typically due to a decrease in blood flow to the dominant hemisphere of the brain and particularly the parietal and premotor areas. It is frequently seen in patients with corticobasal degeneration.

Ideational apraxia has been observed in patients with lesions in the dominant hemisphere near areas associated with aphasia; however, more research is needed on ideational apraxia due to brain lesions. The localization of lesions in areas of the frontal and temporal lobes would provide explanation for the difficulty in motor planning seen in ideational apraxia as well as its difficulty to distinguish it from certain aphasias.

Constructional apraxia is often caused by lesions of the inferior non-dominant parietal lobe, and can be caused by brain injury, illness, tumor or other condition that can result in a brain lesion.

Dysarthria is a motor speech disorder resulting from neurological injury of the motor component of the motor-speech system and is characterized by poor articulation of phonemes. In other words, it is a condition in which problems effectively occur with the muscles that help produce speech, often making it very difficult to pronounce words. It is unrelated to problems with understanding language (that is aphasia), although a person can have both. Any of the speech subsystems (respiration, phonation, resonance, prosody, and articulation) can be affected, leading to impairments in intelligibility, audibility, naturalness, and efficiency of vocal communication. Dysarthria that has progressed to a total loss of speech is referred to as anarthria.

Neurological injury due to damage in the central or peripheral nervous system may result in weakness, paralysis, or a lack of coordination of the motor-speech system, producing dysarthria. These effects in turn hinder control over the tongue, throat, lips or lungs; for example, swallowing problems (dysphagia) are also often present in those with dysarthria.

Dysarthria does not include speech disorders from structural abnormalities, such as cleft palate, and must not be confused with apraxia of speech, which refers to problems in the planning and programming aspect of the motor-speech system. Just as the term "articulation" can mean either "speech" or "joint movement", so is the combining form of the same in the terms "dysarthria", "dysarthrosis", and "arthropathy"; the term "dysarthria" is conventionally reserved for the speech problem and is not used to refer to arthropathy, whereas "dysarthrosis" has both senses but usually refers to arthropathy.

Cranial nerves that control the muscles relevant to dysarthria include the trigeminal nerve's motor branch (V), the facial nerve (VII), the glossopharyngeal nerve (IX), the vagus nerve (X), and the hypoglossal nerve (XII). The term is from New Latin, "dys-" "dysfunctional, impaired" and "arthr-" "joint, vocal articulation")

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.

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.

The prognosis for individuals with apraxia varies. With therapy, some patients improve significantly, while others may show very little improvement. Some individuals with apraxia may benefit from the use of a communication aid.

However, many people with apraxia are no longer able to be independent. Those with limb-kinetic and/or gait apraxia should avoid activities in which they might injure themselves or others.

Occupational therapy, physical therapy, and play therapy may be considered as other references to support patients with apraxia. These team members could work along with the SLP to provide the best therapy for people with apraxia. However, because people with limb apraxia may have trouble directing their motor movements, occupational therapy for stroke or other brain injury can be difficult.

No medication has been shown useful for treating apraxia.

Echolalia (also known as echologia or echophrasia) is defined as the unsolicited repetition of vocalizations made by another person (by the same person is called palilalia). In its profound form it is automatic and effortless. It is one of the echophenomena, closely related to echopraxia, the automatic repetition of movements made by another person; both are "subsets of imitative behavior" whereby sounds or actions are imitated "without explicit awareness". Echolalia may be an immediate reaction to a stimulus or may be delayed.

The word "echolalia" is derived from the Greek , meaning "echo" or "to repeat", and ("laliá") meaning "speech" or "talk" (of onomatopoeic origin, from the verb ("laléo"), meaning "to talk").

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.

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.

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.

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.

Akinetic mutism is a symptom during the final stages of Creutzfeldt–Jakob disease (a rare degenerative brain disease) and can help diagnose patients with this disease. It can also occur in a stroke that affects both anterior cerebral artery territories. Another cause is neurotoxicity due to exposure to certain drugs such as tacrolimus and cyclosporine.

Other causes of akinetic mutism are as follows:

- Respiratory arrest and cerebral hypoxia

- Acute cases of encephalitis lethargica

- Meningitis

- Hydrocephalus

- Trauma

- Tumors

- Aneurysms

- Olfactory groove meningioma

- Cyst in third ventricle

- Toxical lesions and infections of central nervous system

- Delayed post-hypoxic leukoencephalopathy (DPHL)

- Creutzfeldt–Jakob disease (mesencephalic form)

It has long been noted that males are more affected by DLD than females, with a sex ratio of affected males: females around 3 or 4:1 However, the sex difference is much less striking in epidemiological samples, suggesting that similar problems may exist in females but are less likely to be detected. The reason for the sex difference is not well understood.

Poor motor skills are commonly found in children with DLD.

Brain scans do not usually reveal any obvious abnormalities in children with DLD, although quantitative comparisons have found differences in brain size or relative proportions of white or grey matter in specific regions. In some cases, unusual brain gyri are found. To date, no consistent 'neural signature' for DLD has been found, although some studies have noted evidence for involvement of subcortical systems. Differences in the brains of children with DLD vs typically developing children are subtle and may overlap with atypical patterns seen in other neurodevelopmental disorders.

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)

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.

Developmental coordination disorder (DCD), also known as developmental dyspraxia or simply dyspraxia, is a chronic neurological disorder beginning in childhood. It is also known to affect planning of movements and co-ordination as a result of brain messages not being accurately transmitted to the body. Impairments in skilled motor movements per a child's chronological age which must interfere with activities of daily living. A diagnosis of DCD is then reached only in the absence of other neurological impairments like cerebral palsy, muscular dystrophy, multiple sclerosis or Parkinson's disease. According to CanChild in Canada, this disorder affects 5 to 6 percent of school-aged children; however this disorder does progress towards adulthood, therefore making it a lifelong condition.

Stuttering, also known as stammering, is a speech disorder in which the flow of speech is disrupted by involuntary repetitions and prolongations of sounds, syllables, words or phrases as well as involuntary silent pauses or blocks in which the person who stutters is unable to produce sounds. The term "stuttering" is most commonly associated with involuntary sound repetition, but it also encompasses the abnormal hesitation or pausing before speech, referred to by people who stutter as "blocks", and the prolongation of certain sounds, usually vowels or semivowels. According to Watkins et al., stuttering is a disorder of "selection, initiation, and execution of motor sequences necessary for fluent speech production." For many people who stutter, repetition is the primary problem. The term "stuttering" covers a wide range of severity, encompassing barely perceptible impediments that are largely cosmetic to severe symptoms that effectively prevent oral communication. In the world, approximately four times as many men as women stutter, encompassing 70 million people worldwide, or about 1% of the world's population.

The impact of stuttering on a person's functioning and emotional state can be severe. This may include fears of having to enunciate specific vowels or consonants, fears of being caught stuttering in social situations, self-imposed isolation, anxiety, stress, shame, being a possible target of bullying (especially in children), having to use word substitution and rearrange words in a sentence to hide stuttering, or a feeling of "loss of control" during speech. Stuttering is sometimes popularly seen as a symptom of anxiety, but there is actually no direct correlation in that direction (though as mentioned the inverse can be true, as social anxiety may actually develop in individuals as a result of their stuttering).

Stuttering is generally not a problem with the physical production of speech sounds or putting thoughts into words. Acute nervousness and stress do not cause stuttering, but they can trigger stuttering in people who have the speech disorder, and living with a stigmatized disability can result in anxiety and high allostatic stress load (chronic nervousness and stress) that reduce the amount of acute stress necessary to trigger stuttering in any given person who stutters, exacerbating the problem in the manner of a positive feedback system; the name 'stuttered speech syndrome' has been proposed for this condition. Neither acute nor chronic stress, however, itself creates any predisposition to stuttering.

The disorder is also "variable", which means that in certain situations, such as talking on the telephone or in a large group, the stuttering might be more severe or less, depending on whether or not the stutterer is self-conscious about their stuttering. Stutterers often find that their stuttering fluctuates and that they have "good" days, "bad" days and "stutter-free" days. The times in which their stuttering fluctuates can be random. Although the exact etiology, or cause, of stuttering is unknown, both genetics and neurophysiology are thought to contribute. There are many treatments and speech therapy techniques available that may help decrease speech disfluency in some people who stutter to the point where an untrained ear cannot identify a problem; however, there is essentially no cure for the disorder at present. The severity of the person's stuttering would correspond to the amount of speech therapy needed to decrease disfluency. For severe stuttering, long-term therapy and hard work is required to decrease disfluency.

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)