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 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.

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")

There are two types of Apraxia. Developmental (or Childhood Apraxia of speech) or acquired Apraxia. Childhood apraxia of speech (CAS) is a neurological childhood speech sound disorder that involves impaired precision and consistency of movements required for speech production without any neuromuscular deficits (ASHA, 2007a, Definitions of CAS section, para. 1). Both are the inability to plan volitional motor movements for speech production in the absence of muscular weakness. Apraxia is not a result of sensory problems, or physical issues with the articulatory structures themselves, simply the way the brain plans to move them.

There are several types of apraxia including:

- Ideomotor apraxia: These patients have deficits in their ability to plan or complete motor actions that rely on semantic memory. They are able to explain how to perform an action, but unable to "imagine" or act out a movement such as "pretend to brush your teeth" or "pucker as though you bit into a sour lemon." However, when the ability to perform an action automatically when cued remains intact, this is known as automatic-voluntary dissociation. For example, they may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings.

- Ideational/conceptual apraxia: Patients have an inability to conceptualize a task and impaired ability to complete multistep actions. Consists of an inability to select and carry out an appropriate motor program. For example, the patient may complete actions in incorrect orders, such as buttering bread before putting it in the toaster, or putting on shoes before putting on socks. There is also a loss of ability to voluntarily perform a learned task when given the necessary objects or tools. For instance, if given a screwdriver, the patient may try to write with it as if it were a pen, or try to comb his hair with a toothbrush.

- Buccofacial or orofacial apraxia: Non-verbal oral or buccofacial ideomotor apraxia describes difficulty carrying out movements of the face on demand. For example, an inability to lick one's lips or whistle when requested suggests an inability to carry out volitional movements of the tongue, cheeks, lips, pharynx, or larynx on command.

- Constructional apraxia: The inability to draw or construct simple configurations, such as intersecting shapes.

- Gait apraxia: The loss of ability to have normal function of the lower limbs such as walking. This is not due to loss of motor or sensory functions.

- Limb-kinetic apraxia: voluntary movements of extremities are impaired. For example, a person affected by limb apraxia may have difficulty waving hello.

- Oculomotor apraxia: Difficulty moving the eye, especially with saccade movements that direct the gaze to targets. This is one of the 3 major components of Balint's syndrome.

- Apraxia of speech (AOS): Difficulty planning and coordinating the movements necessary for speech (e.g. Potato=Totapo, Topato.) AOS can independently occur without issues in areas such as verbal comprehension, reading comprehension, writing, articulation or prosody.

Ideomotor apraxia (IMA) impinges on one's ability to carry out common, familiar actions on command, such as waving goodbye. Persons with IMA exhibit a loss of ability to carry out motor movements, and may show errors in how they hold and move the tool in attempting the correct function.

One of the defining symptoms of ideomotor apraxia is the inability to pantomime tool use. As an example, if a normal individual were handed a comb and instructed to pretend to brush his hair, he would grasp the comb properly and pass it through his hair. If this were repeated in a patient with ideomotor apraxia, the patient may move the comb in big circles around his head, hold it upside-down, or perhaps try and brush his teeth with it. The error may also be temporal in nature, such as brushing exceedingly slowly. The other characteristic symptom of ideomotor apraxia is the inability to imitate hand gestures, meaningless or meaningful, on request; a meaningless hand gesture is something like having someone make a ninety-degree angle with his thumb and placing it under his nose, with his hand in the plane of his face. This gesture has no meaning attached to it. In contrast, a meaningful gesture is something like saluting or waving goodbye. An important distinction here is that all of the above refer to actions that are consciously and voluntarily initiated. That is to say that a person is specifically asked to either imitate what someone else is doing or is given verbal instructions, such as "wave goodbye." People suffering from ideomotor apraxia will know what they are supposed to do, e.g. they will know to wave goodbye and what their arm and hand should do to accomplish it, but will be unable to execute the motion correctly. This voluntary type of action is distinct from spontaneous actions. Ideomotor apraxia patients may still retain the ability to perform spontaneous motions; if someone they know leaves the room, for instance, they may be able to wave goodbye to that person, despite being unable to do so at request. The ability to perform this sort of spontaneous action is not always retained, however; some sufferers lose this capability, as well. The recognition of meaningful gestures, e.g. understanding what waving goodbye means when it is seen, seems to be unaffected by ideomotor apraxia. It has also been shown that ideomotor apraxia sufferers may have some deficits in general spontaneous movements. Apraxia patients appear to be unable to tap their fingers as quickly as a control group, with a lower maximum tapping rate correlated with more severe apraxia. It has also been demonstrated that apraxic patients are slower to point at a target light when they do not have sight of their hand as compared with healthy patients under the same conditions. The two groups did not differ when they could see their hands. The speed and accuracy of grasping objects also appears unaffected by ideomotor apraxia. Patients suffering from ideomotor apraxia appear to be much more reliant on visual input when conducting movements then nonapraxic individuals.

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.

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex), in which the individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and he/she is willing to perform the task. The nature of the brain damage determines the severity, and the absence of sensory loss or paralysis helps to explain the level of difficulty.

The term comes from the Greek ἀ- "a-" ("without") and πρᾶξις "praxis" ("action").

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.

Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.

- Difficulty in initiating movement

- Poor truncal mobility

- Falls due to minor balance disturbances

- Greatly hindered postural responses

- Characteristic magnetic gait, the inability to raise one's foot off of the floor.

- Wide base, poor balance control when in stance

- Short stride

- En bloc turns

Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs (Plantar reflex). Urinary incontinence may also be present.

Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia.

Ideomotor Apraxia, often IMA, is a neurological disorder characterized by the inability to correctly imitate hand gestures and voluntarily mime tool use, e.g. pretend to brush one's hair. The ability to spontaneously use tools, such as brushing one's hair in the morning without being instructed to do so, may remain intact, but is often lost. The general concept of apraxia and the classification of ideomotor apraxia were developed in Germany in the late 19th and early 20th centuries by the work of Hugo Liepmann, Adolph Kussmaul, Arnold Pick, Paul Flechsig, Hermann Munk, Carl Nothnagel, Theodor Meynert, and linguist Heymann Steinthal, among others. Ideomotor apraxia was classified as "ideo-kinetic apraxia" by Liepmann due to the apparent dissociation of the idea of the action with its execution. The classifications of the various subtypes are not well defined at present, however, owing to issues of diagnosis and pathophysiology. Ideomotor apraxia is hypothesized to result from a disruption of the system that relates stored tool use and gesture information with the state of the body to produce the proper motor output. This system is thought to be related to the areas of the brain most often seen to be damaged when ideomotor apraxia is present: the left parietal lobe and the premotor cortex. Little can be done at present to reverse the motor deficit seen in ideomotor apraxia, although the extent of dysfunction it induces is not entirely clear.

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.

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.

Bruns apraxia, or frontal ataxia is a gait apraxia found in patients with bilateral frontal lobe disorders. It is characterised by an inability to initiate the process of walking, despite the power and coordination of the legs being normal when tested in the seated or lying position. The gait is broad-based with short steps with a tendency to fall backwards. It was originally described in patients with frontal lobe tumours, but is now more commonly seen in patients with cerebrovascular disease.

It is named after Ludwig Bruns.

Various areas of development can be affected by developmental coordination disorder and these will persist into adulthood, as DCD has no cure. Often various coping strategies are developed, and these can be enhanced through occupational therapy, psychomotor therapy, physiotherapy, speech therapy, or psychological training.

In addition to the physical impairments, developmental coordination disorder is associated with problems with memory, especially working memory. This typically results in difficulty remembering instructions, difficulty organizing one's time and remembering deadlines, increased propensity to lose things or problems carrying out tasks which require remembering several steps in sequence (such as cooking). Whilst most of the general population experience these problems to some extent, they have a much more significant impact on the lives of dyspraxic people. However, many dyspraxics have excellent long-term memories, despite poor short-term memory. Many dyspraxics benefit from working in a structured environment, as repeating the same routine minimises difficulty with time-management and allows them to commit procedures to long-term memory.

People with developmental coordination disorder sometimes have difficulty moderating the amount of sensory information that their body is constantly sending them, so as a result dyspraxics are prone to sensory overload and panic attacks.

Many dyspraxics struggle to distinguish left from right, even as adults, and have extremely poor sense of direction generally.

Moderate to extreme difficulty doing physical tasks is experienced by some dyspraxics, and fatigue is common because so much extra energy is expended while trying to execute physical movements correctly. Some (but not all) dyspraxics suffer from hypotonia, low muscle tone, which like DCD can detrimentally affect balance.

Fine-motor problems can cause difficulty with a wide variety of other tasks such as using a knife and fork, fastening buttons and shoelaces, cooking, brushing one's teeth, styling one's hair, shaving, applying cosmetics, opening jars and packets, locking and unlocking doors, and doing housework.

Difficulties with fine motor co-ordination lead to problems with handwriting, which may be due to either ideational or ideo-motor difficulties.

Problems associated with this area may include:

- Learning basic movement patterns.

- Developing a desired writing speed.

- Establishing the correct pencil grip

- The acquisition of graphemes – e.g. the letters of the Latin alphabet, as well as numbers.

Oculomotor apraxia (OMA), also known as Cogan ocular motor apraxia or saccadic initiation failure (SIF) is the absence or defect of controlled, voluntary, and purposeful eye movement. It was first described in 1952 by the American ophthalmologist David Glendenning Cogan. People with this condition have difficulty moving their eyes horizontally and moving them quickly. The main difficulty is in saccade initiation, but there is also impaired cancellation of the vestibulo-ocular reflex. Patients have to turn their head in order to compensate for the lack of eye movement initiation in order to follow an object or see objects in their peripheral vision, but they often exceed their target. There is controversy regarding whether OMA should be considered an apraxia, since apraxia is the inability to perform a learned or skilled motor action to command, and saccade initiation is neither a learned nor a skilled action.

Damage to the cerebellum, particularly to the cerebrocerebellum area and the cerebellar vermis, is very often associated with clinical depression and often with alcoholism. Due to difficulties in mobility, self-care, everyday activities, and pain/discomfort, those with cerebellar ataxia are more likely to be diagnosed with anxiety and depression. Almost a third of patients with isolated, late onset cerebellar ataxia go on to develop multiple system atrophy.

In recent years the cerebellum's role has been observed as not purely motor. It is intimately combined with intellect, emotion and planning.

Speech and language impairment are basic categories that might be drawn in issues of communication involve hearing, speech, language, and fluency.

A speech impairment is characterized by difficulty in articulation of words. Examples include stuttering or problems producing particular sounds. Articulation refers to the sounds, syllables, and phonology produced by the individual. Voice, however, may refer to the characteristics of the sounds produced—specifically, the pitch, quality, and intensity of the sound. Often, fluency will also be considered a category under speech, encompassing the characteristics of rhythm, rate, and emphasis of the sound produced

A language impairment is a specific impairment in understanding and sharing thoughts and ideas, i.e. a disorder that involves the processing of linguistic information. Problems that may be experienced can involve the form of language, including grammar, morphology, syntax; and the functional aspects of language, including semantics and pragmatics

An individual can have one or both types of impairment. These impairments/disorders are identified by a speech and language pathologist.

Even though OMA is not always associated with developmental issues, children with this condition often have hypotonia, decreased muscle tone, and show developmental delays. Some common delays are seen in speech, reading and motor development

Gerstmann syndrome is characterized by four primary symptoms:

1. Dysgraphia/agraphia: deficiency in the ability to write

2. Dyscalculia/acalculia: difficulty in learning or comprehending mathematics

3. Finger agnosia/anomia: inability to distinguish the fingers on the hand

4. Left-right disorientation

The main clinical features are signature language progressive difficulties with speech production. There can be problems in different parts of the speech production system, hence patients can present with articulatory breakdown, phonemic breakdown (difficulties with sounds) and other problems. However, it is rare for patients to have just one of these problems and most people will present with more than one problem. Features include:

- Hesitant, effortful speech

- Speech 'apraxia'

- Stutter (including return of a childhood stutter)

- Anomia

- Phonemic paraphasia (sound errors in speech e.g. 'gat' for 'cat')

- Agrammatism (using the wrong tense or word order)

As the disease develops, speech quantity decreases and many patients will become mute.

Cognitive domains other than language are rarely affected early on. However, as the disease progresses other domains can be affected. Problems with writing, reading and speech comprehension can occur as can behavioural features similar to frontotemporal dementia.

Motor disorders are malfunctions of the nervous system that cause involuntary or uncontrollable movements or actions of the body (Stone). These disorders can cause lack of intended movement or an excess of involuntary movement (Mandal). Symptoms of motor disorders include tremors, jerks, twitches, spasms, contractions, or gait problems.

Tremor is the uncontrollable shaking of an arm or a leg. Twitches or jerks of body parts may occur due to a startling sound or unexpected, sudden pain. Spasms and contractions are temporary abnormal resting positions of hands or feet. Spasms are temporary while contractions could be permanent. Gait problems are problems with the way one walks or runs. This can mean an unsteady pace or dragging of the feet along with other possible irregularities (Stone).