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.

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")

Dysarthria is the reduced ability to motor plan volitional movements needed for speech production as the result of weakness/paresis and/or paralysis of the musculature of the oral mechanism needed for respiration, phonation, resonance, articulation, and/or prosody.

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.

Cerebellar ataxia can occur as a result of many diseases and presents with symptoms of an inability to coordinate balance, gait, extremity and eye movements. Lesions to the cerebellum can cause dyssynergia, dysmetria, dysdiadochokinesia, dysarthria and ataxia of stance and gait. Deficits are observed with movements on the same side of the body as the lesion (ipsilateral). Clinicians often use visual observation of people performing motor tasks in order to look for signs of ataxia.

ADCP is often characterized by slow, uncontrolled movements of the extremities and trunk. Small, rapid, random and repetitive, uncontrolled movements known as chorea may also occur. Involuntary movements often increase during periods of emotional stress or excitement and disappear when the patient is sleeping or distracted. Patients experience difficulty in maintaining posture and balance when sitting, standing, and walking due to these involuntary movements and fluctuations in muscle tone. Coordinated activities such as reaching and grasping may also be challenging. Muscles of the face and tongue can be affected, causing involuntary facial grimaces, expressions, and drooling. Speech and language disorders, known as dysarthria, are common in athetoid CP patients. In addition, ADCP patients may have trouble eating. Hearing loss is a common co-occurring condition, and visual disabilities can be associated with Athetoid Cerebral Palsy. Squinting and uncontrollable eye movements may be initial signs and symptoms. Children with these disabilities rely heavily on visual stimulation, especially those who are also affected by sensory deafness.

Cognitive impairment occur in 30% of cases.

Epilepsy occur in 25% of cases.

AOS and expressive aphasia (also known as Broca's aphasia) are commonly mistaken as the same disorder mainly because they often occur together in patients. Although both disorders present with symptoms such as a difficulty producing sounds due to damage in the language parts of the brain, they are not the same. The main difference between these disorders lies in the ability to comprehend spoken language; patients with apraxia are able to fully comprehend speech, while patients with aphasia are not always fully able to comprehend others' speech.

Conduction aphasia is another speech disorder that is similar to, but not the same as, apraxia of speech. Although patients who suffer from conduction aphasia have full comprehension of speech, as do AOS sufferers, there are differences between the two disorders. Patients with conduction aphasia are typically able to speak fluently, but they do not have the ability to repeat what they hear.

Similarly, dysarthria, another motor speech disorder, is characterized by difficulty articulating sounds. The difficulty in articulation does not occur due in planning the motor movement, as happens with AOS. Instead, dysarthria is caused by inability in or weakness of the muscles in the mouth, face, and respiratory system.

Apraxia of speech (AOS) is an acquired oral motor speech disorder affecting an individual's ability to translate conscious speech plans into motor plans, which results in limited and difficult speech ability. By the definition of apraxia, AOS affects volitional (willful or purposeful) movement patterns, however AOS usually also affects automatic speech.

Individuals with AOS have difficulty connecting speech messages from the brain to the mouth. AOS is a loss of prior speech ability resulting from a brain injury such as a stroke or progressive illness.

Developmental verbal dyspraxia (DVD), also known as childhood apraxia of speech (CAS) and developmental apraxia of speech (DAS); is an inability to utilize motor planning to perform movements necessary for speech during a child's language learning process. Although the causes differ between AOS and DVD, the main characteristics and treatments are similar.

Palilalia is considered an aphasia, a disorder of language, and is not to be confused with speech disorders, as there is no difficulty in the formation of internal speech. Palilalia is similar to speech disorders such as stuttering or cluttering, as it tends to only express itself in spontaneous speech, such as answering basic questions, and not in automatic speech such as reading or singing; however, it distinctively affects words and phrases rather than syllables and sounds.

Palilalia may occur in conditions affecting the pre-frontal cortex or basal ganglia regions, either from physical trauma, neurodegenerative disorders, genetic disorders, or a loss of dopamine in these brain regions. Palilalia occurs most commonly in Tourette syndrome and may be present in neurodegenerative disorders like Alzheimer's disease and progressive supranuclear palsy.

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.

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.

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.

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.

Signs and symptoms of pseudobulbar palsy include:

- Slow and indistinct speech

- Dysphagia (difficulty in swallowing)

- Small, stiff and spastic tongue

- Brisk jaw jerk

- Dysarthria

- Labile affect

- Gag reflex may be normal, exaggerated or absent

- Examination may reveal upper motor neuron lesion of the limbs

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.

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.

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.

Athetoid cerebral palsy or dyskinetic cerebral palsy (sometimes abbreviated ADCP) is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic-ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

Classification of cerebral palsy can be based on severity, topographic distribution, or motor function. Severity is typically assessed via the Gross Motor Function Classification System (GMFCS) or the International Classification of Functioning, Disability and Health (described further below). Classification based on motor characteristics classifies CP as occurring from damage to either the corticospinal pathway or extrapyramidal regions. Athetoid dyskinetic cerebral palsy is a non-spastic, extrapyramidal form of cerebral palsy (spastic cerebral palsy, in contrast, results from damage to the brain’s corticospinal pathways). Non-spastic cerebral palsy is divided into two groups, ataxic and dyskinetic. Dyskinetic cerebral palsy is separated further into two different groups; choreoathetoid and dystonic. Choreo-athetotic CP is characterized by involuntary movements most predominantly found in the face and extremities. Dystonic ADCP is characterized by slow, strong contractions, which may occur locally or encompass the whole body.

Clinically, physicians have also classified cerebral palsy according to the topographic distribution of muscle spasticity. This method classifies children as diplegic, (bilateral involvement with leg involvement greater than arm involvement), hemiplegic (unilateral involvement), or quadriplegic (bilateral involvement with arm involvement equal to or greater than leg involvement).

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.

After experiencing brain injury, some people may begin speaking in an accent not native to their country of origin, as discussed in the preceding sections, but more common forms of dysprosody consist of alterations in vocal pitch, timing, rhythm, and control, not necessarily resulting in a foreign dialect. In addition, there have been some cases in which seizures began to develop in patients also suffering from dysprosody, but no decisive conclusions connecting dysprosody and seizure activity have been made.

Dysprosody can last for differing durations, from a few months to years, although the reason seems to be unclear.

There are several different types of dysprosody which have been classified. The most common types of dysprosody are associated with dysarthria and developmental coordination disorder, which affect motor processing in speech. Among the most studied types are:

- Flaccid dysarthria is characterized by little control over pitch and voice volume, reduced speech rate, and impaired voice quality

- Hypokinetic dysarthria is characterized by harsh voice quality, monotone, reduced volume and breathiness

- Ataxic dysarthria is characterized by harsh voice quality, reduced speech rate, and poor volume and pitch control

- Developmental verbal dyspraxia is characterized by monotone and poor volume control

There can also be some emotional and mental side effects to dysprosody. Each individual has a distinct voice characterized by all the prosodic elements. Once a person loses control of the timing, pitch, melody, etc. of his speech, he can also feel a sense of loss of personal identity, which can sometimes lead to depression.

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.

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).

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.

The initial symptoms in two-thirds of cases are loss of balance, lunging forward when mobilizing, fast walking, bumping into objects or people, and falls.

Other common early symptoms are changes in personality, general slowing of movement, and visual symptoms.

Later symptoms and signs are dementia (typically including loss of inhibition and ability to organize information), slurring of speech, difficulty swallowing, and difficulty moving the eyes, particularly in the vertical direction. The latter accounts for some of the falls experienced by these patients as they are unable to look up or down.

Some of the other signs are poor eyelid function, contracture of the facial muscles, a backward tilt of the head with stiffening of the , sleep disruption, urinary incontinence and constipation.

The visual symptoms are of particular importance in the diagnosis of this disorder. Patients typically complain of difficulty reading due to the inability to look down well. Notably, the ophthalmoparesis experienced by these patients mainly concerns voluntary eye movement and the inability to make vertical saccades, which is often worse with downward saccades. Patients tend to have difficulty looking down (a downgaze ) followed by the addition of an upgaze palsy. This vertical gaze paresis will correct when the examiner passively rolls the patient's head up and down as part of a test for the oculocephalic reflex. Involuntary eye movement, as elicited by Bell's phenomenon, for instance, may be closer to normal. On close inspection, eye movements called "square-wave jerks" may be visible when the patient fixes at distance. These are fine movements, that can be mistaken for nystagmus, except that they are saccadic in nature, with no smooth phase. Difficulties with convergence (convergence insufficiency), where the eyes come closer together while focusing on something near, like the pages of a book, is typical. Because the eyes have trouble coming together to focus at short distances, the patient may complain of diplopia (double vision) when reading.

Cardinal manifestations:

- Supranuclear ophthalmoplegia

- Neck dystonia

- Parkinsonism

- Pseudobulbar palsy

- Behavioral and cognitive impairment

- Imbalance and walking difficulty

- Frequent falls

Even though most speech sound disorders can be successfully treated in childhood, and a few may even outgrow them on their own, errors may sometimes persist into adulthood rather than only being not age appropriate. Such persisting errors are referred to as "residual errors" and may remain for life.