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

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.

The severity of impairment and related prognosis is dependent on the location and severity of brain lesions. Up to 50% of patients will achieve some degree of ambulation. Speech problems, such as dysarthria, are common to these patients.

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.

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.

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.

CP in general is a non-progressive, neurological condition that results from brain injury and malformation occurring before cerebral development is complete. ADCP is associated with injury and malformations to the extrapyramidal tracts in the basal ganglia or the cerebellum. Lesions to this region principally arise via hypoxic ischemic brain injury (HIBI) or bilirubin encephalopathy.

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.

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.

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.

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.

There are many causes of cerebellar ataxia including, among others, gluten ataxia, autoimmunity to Purkinje cells or other neural cells in the cerebellum, CNS vasculitis, multiple sclerosis, infection, bleeding, infarction, tumors, direct injury, toxins (e.g., alcohol), genetic disorders, and an association with statin use. Gluten ataxia accounts for 40% of all sporadic idiopathic ataxias and 15% of all ataxias.

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.

Pseudobulbar palsy is the result of damage of motor fibers traveling from the cerebral cortex to the lower brain stem. This damage might arise in the course of a variety of neurological conditions that involve demyelination and bilateral corticobulbar lesions. Examples include:

- Vascular causes: bilateral hemisphere infarction, CADASIL syndrome

- Progressive supranuclear palsy

- Amyotrophic lateral sclerosis

- Parkinson's disease and related multiple system atrophy

- Various motor neuron diseases, especially those involving demyelination

- Multiple sclerosis and other inflammatory disorders

- High brain stem tumors

- Metabolic causes: osmotic demyelination syndrome

- Neurological involvement in Behçet's disease

- Brain trauma

The proposed mechanism of pseudobulbar palsy points to the disinhibition of the motor neurons controlling laughter and crying, proposing that a reciprocal pathway exists between the cerebellum and the brain stem that adjusts laughter and crying responses, making them appropriate to context. The pseudobulbar crying could also be induced by stimulation in the region of the subthalamic nucleus of the brain.

Cerebellar ataxia is a form of ataxia originating in the cerebellum. Non-progressive congenital ataxia (NPCA) is a classical presentation of cerebral ataxias.

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.

Dysdiadochokinesia, dysdiadochokinesis, dysdiadokokinesia, dysdiadokokinesis (from Greek "δυς" "dys" "bad", "διάδοχος" "diadochos" "succeeding", "κίνησις" "kinesis" "movement"), often abbreviated as DDK, is the medical term for an impaired ability to perform rapid, alternating movements (i.e., diadochokinesia). Complete inability is called adiadochokinesia.

Spasmodic torticollis is one of the most common forms of dystonia seen in neurology clinics, occurring in approximately 0.390% of the United States population in 2007 (390 per 100,000). Worldwide, it has been reported that the incidence rate of spasmodic torticollis is at least 1.2 per 100,000 person years, and a prevalence rate of 57 per 1 million.

The exact prevalence of the disorder is not known; several family and population studies show that as many as 25% of cervical dystonia patients have relatives that are undiagnosed. Studies have shown that spasmodic torticollis is not diagnosed immediately; many patients are diagnosed well after a year of seeking medical attention. A survey of 59 patients diagnosed with spasmodic torticollis show that 43% of the patients visited at least four physicians before the diagnosis was made.

There is a higher prevalence of spasmodic torticollis in females; females are 1.5 times more likely to develop spasmodic torticollis than males. The prevalence rate of spasmodic torticollis also increases with age, most patients show symptoms from ages 50–69. The average onset age of spasmodic torticollis is 41.

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.

Dysdiadochokinesia is a feature of cerebellar ataxia and may be the result of lesions to either the cerebellar hemispheres or the frontal lobe (of the cerebrum), it can also be a combination of both. It is thought to be caused by the inability to switch on and switch off antagonising muscle groups in a coordinated fashion due to hypotonia, secondary to the central lesion.

Dysdiadochokinesia is also seen in Friedreich's ataxia and multiple sclerosis, as a cerebellar symptom (including ataxia, intention tremor and dysarthria). It is also a feature of ataxic dysarthria. Dysdiadochokinesia often presents in motor speech disorders (dysarthria), therefore testing for dysdiadochokinesia can be used for a differential diagnosis.

Dysdiadochokinesia has been linked to a mutation in "SLC18A2", which encodes vesicular monoamine transporter 2 (VMAT2).

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.

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.

When other conditions lead to spasmodic torticollis, it is said that the spasmodic torticollis is secondary. A variety of conditions can cause brain injury, from external factors to diseases. These conditions are listed below:

- Perinatal (during birth) cerebral injury

- Kernicterus

- Cerebrovascular diseases

- Drug induced

- Central nervous system tumor

- Peripheral or central trauma

- Infectious or post infectious encephalopathies

- Toxins

- Metabolic

- Paraneoplastic syndromes

- Central pontine myelinolysis

Secondary spasmodic torticollis is diagnosed when any of the following are present: history of exogenous insult or exposure, neurological abnormalities other than dystonia, abnormalities on brain imaging, particularly in the basal ganglia.

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.