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.

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.

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.

Broca's (expressive) aphasia is a type of non-fluent aphasia in which an individual’s speech is halting and effortful. Misarticulations or distortions of consonants and vowels, namely phonetic dissolution, are common. Individuals with expressive aphasia may only produce single words, or words in groups of two or three. Long pauses between words are common and multi-syllabic words may be produced one syllable at a time with pauses between each syllable. The prosody of a person with Broca's aphasia is compromised by shortened length of utterances and the presence of self-repairs and disfluencies. Intonation and stress patterns are also deficient.

For example, in the following passage, a patient with Broca's aphasia is trying to explain how he came to the hospital for dental surgery and it may look like this:Yes... ah... Monday... er... Dad and Peter H... (his own name), and Dad... er... hospital... and ah... Wednesday... Wednesday, nine o'clock... and oh... Thursday... ten o'clock, ah doctors... two... an' doctors... and er... teeth... yah.The speech of a person with expressive aphasia contains mostly content words such as nouns, verbs, and some adjectives. However, function words like conjunctions, articles, and prepositions are rarely used except for “and” which is prevalent in the speech of most patients with aphasia. The omission of function words makes the person's speech agrammatic. A communication partner of a person with aphasia may say that the person's speech sounds telegraphic due to poor sentence construction and disjointed words. For example, a person with expressive aphasia might say "Smart... university... smart... good... good..."

Self-monitoring is typically well preserved in patients with Broca's aphasia. They are usually aware of their communication deficits, and are more prone to depression and outbursts from frustration than are patients with other forms of aphasia.

In general, word comprehension is preserved, allowing patients to have functional receptive language skills. Individuals with Broca's aphasia understand most of the everyday conversation around them, but higher-level deficits in receptive language can occur. Because comprehension is substantially impaired for more complex sentences, it is better to use simple language when speaking with an individual with expressive aphasia. This is exemplified by the difficulty to understand phrases or sentences with unusual structure. A typical patient with Broca's aphasia will misinterpret "the man is bitten by the dog" by switching the subject and object to “the dog is bitten by the man.”

Typically, people with expressive aphasia can understand speech and read better than they can produce speech and write. The person's writing will resemble his or her speech and will be effortful, lacking cohesion, and containing mostly content words. Letters will likely be formed clumsily and distorted and some may even be omitted. Although listening and reading are generally intact, subtle deficits in both reading and listening comprehension are almost always present during assessment of aphasia.

Because Broca's area is anterior to the primary motor cortex which is responsible for movement of the face, hands, and arms, a lesion affecting Broca's areas may also result in hemiparesis (weakness of both limbs on the same side of the body) or hemiplegia (paralysis of both limbs on the same side of the body). The brain is wired contralaterally, which means the limbs on right side of the body are controlled by the left hemisphere and vice versa. Therefore, when Broca's area or surrounding areas in the left hemisphere are damaged, hemiplegia or hemiparesis often occurs on the right side of the body in individuals with Broca's aphasia.

Severity of expressive aphasia varies among patients. Some people may only have mild deficits and detecting problems with their language may be difficult. In the most extreme cases, patients may be able to produce only a single word. Even in such cases, over-learned and rote-learned speech patterns may be retained- for instance, some patients can count from one to ten, but cannot produce the same numbers in novel conversation.

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").

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.

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.

Peripheral agraphias occurs when there is damage to the various motor and visualization skills involved in writing.

- Apraxic agraphia is the impairment in written language production associated with disruption of the motor system. It results in distorted, slow, effortful, incomplete, and/or imprecise letter formation. Though written letters are often so poorly formed that they are almost illegible, the ability to spell aloud is often retained. This form of agraphia is caused specifically by a loss of specialized motor plans for the formation of letters and not by any dysfunction affecting the writing hand. Apraxic agraphia may present with or without ideomotor apraxia. Paralysis, chorea, Parkinson's disease (micrographia), and dystonia (writer's cramp) are motor disorders commonly associated with agraphia.

- Hysterical agraphia is the impairment in written language production caused by a conversion disorder.

- Reiterative agraphia is found in individuals who repeat letters, words, or phrases in written language production an abnormal number of times. Preservation, paragraphia, and echographia are examples of reiterative agraphia.

- Visuospatial agraphia is the impairment in written language production defined by a tendency to neglect one portion (often an entire side) of the writing page, slanting lines upward or downward, and abnormal spacing between letters, syllables, and words. The orientation and correct sequencing of the writing will also be impaired. Visuospatial agraphia is frequently associated with left hemispatial neglect, difficulty in building or assembling objects, and other spatial difficulties.

It is most common for the onset of global aphasia to occur after a thrombotic stroke (at the trunk of the middle cerebral artery), with varying severity. The general signs and symptoms include the inability to understand, create, and repeat speech and language. These difficulties also persist in reading, writing, and auditory comprehension abilities.

Verbal language typically consists of a few recognizable utterances and words (e.g., hello), overlearned phrases (e.g., how are you), and expletives (e.g., a curse word). However, those affected by global aphasia may express themselves using facial expressions, intonation, and gestures. Extensive lexical (vocabulary) impairment is possible, resulting in an inability to read simple words or sentences. Global aphasia may be accompanied by weakness of the right side of the face and right hemiplegia (paralysis), but can occur with or without hemiparesis (weakness). Additionally, it is common for an individual with global aphasia to have one or more of the following additional impairments: apraxia of speech, alexia, pure word deafness, agraphia, facial apraxia, and depression.

Persons with global aphasia are socially appropriate, usually attentive, and task-oriented. Some are able to respond to yes/no questions, but responses are more reliable when questions refer to family and personal experiences. Automatic speech is preserved with normal phonemic, phonetic and inflectional structures. Right hemiparesis or hemiplegia, right-sided sensory loss, and right homonymous hemianopsia may manifest as well. Persons with global aphasia may recognize location names and common objects’ names (single-words), while rejecting pseudo-words and real but incorrect names.

In addition to difficulty expressing oneself, individuals with expressive aphasia are also noted to commonly have trouble with comprehension in certain linguistic areas. This agrammatism overlaps with receptive aphasia, but can be seen in patients who have expressive aphasia without being diagnosed as having receptive aphasia. The most well-noted of these are object-relative clauses, object Wh- questions, and topicalized structures (placing the topic at the beginning of the sentence). These three concepts all share phrasal movement, which can cause words to lose their thematic roles when they change order in the sentence. This is often not an issue for people without agrammatic aphasias, but many people with aphasia rely heavily on word order to understand roles that words play within the sentence.

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.

Central agraphia occurs when there are both impairments in spoken language and impairments to the various motor and visualization skills involved in writing. Individuals who have agraphia with fluent aphasia write a normal quantity of well-formed letters, but lack the ability to write meaningful words. Receptive aphasia is an example of fluent aphasia. Those who have agraphia with nonfluent aphasia can write brief sentences but their writing is difficult to read. Their writing requires great physical effort but lacks proper syntax and often has poor spelling. Expressive aphasia is an example of nonfluent aphasia. Individuals who have Alexia with agraphia have difficulty with both the production and comprehension of written language. This form of agraphia does not impair spoken language.

- Deep agraphia affects an individuals' phonological ability and orthographic memory. Deep agraphia is often the result of a lesion involving the left parietal region (supramarginal gyrus or insula). Individuals can neither remember how words look when spelled correctly, nor sound them out to determine spelling. Individuals typically rely on their damaged orthographic memory to spell; this results in frequent errors, usually semantic in nature. Individuals have more difficulty with abstract concepts and uncommon words. Reading and spoken language are often impaired as well.

- Gerstmann syndrome agraphia is the impairment of written language production associated with the following structural symptoms: difficulty discriminating between one's own fingers, difficulty distinguishing left from right, and difficulty performing calculations. All four of these symptoms result from pathway lesions. Gerstmann's syndrome may additionally be present with alexia and mild aphasia.

- Global agraphia also impairs an individuals' orthographic memory although to a greater extent than deep agraphia. In global apraxia, spelling knowledge is lost to such a degree that the individual can only write very few meaningful words, or cannot write any words at all. Reading and spoken language are also markedly impaired.

- Lexical and structural agraphia are caused by damage to the orthographic memory; these individuals cannot visualize the spelling of a word, though they do retain the ability to sound them out. This impaired spelling memory can imply the loss or degradation of the knowledge or just an inability to efficiently access it. There is a regularity effect associated with lexical agraphia in that individuals are less likely to correctly spell words without regular, predictable spellings. Additionally, spelling ability tends to be less impaired for common words. Individuals also have difficulty with homophones. Language competence in terms of grammar and sentence writing tends to be preserved.

- Phonological agraphia is the opposite of lexical agraphia in that the ability to sound out words is impaired, but the orthographical memory of words may be intact. It is associated with a lexicality effect by a difference in the ability to spell words versus nonwords; individuals with this form of agraphia are depending on their orthographic memory. Additionally, it is often harder for these individuals to access more abstract words without strong semantic representations (i.e., it is more difficult for them to spell prepositions than concrete nouns).

- Pure agraphia is the impairment in written language production without any other language or cognitive disorder.

Agraphia can occur separately or co-occur and can be caused by damage to the angular gyrus

FCMS shares similar characteristics with the following disorders: catatonia, akinetic mutism, orbuccal apraxia, Broca’s aphasia, pseudobulbar palsy, bulbar palsy secondary to myasthenia gravis, Guillain-Barré syndrome, and brainstem strokes.

In determining a diagnosis between with catatonia, akinetic mutism, and FCMS, a person must demonstrate their ability to perform voluntary function of the limbs. Patients with catatonia or akinetic mutism are not able to perform voluntary commands that involve the use of limbs, while patients with FCMS still possess voluntary usage of limbs. If a person can demonstrate ability in voluntary usage of limbs, catatonia and akinetic mutism are most likely ruled out from the diagnosis.

In determining a diagnosis between Broca’s aphasia and FCMS, a person must demonstrate their ability in voluntary movement of cranial musculature. People with Broca’s aphasia may not exhibit a complete loss of voluntary movement facial muscles, pharyngeal muscles, laryngeal muscles, brachial muscles, tongue muscles, and muscles of the mouth that aid in chewing. These voluntary functions may still be present, to varying degrees. People with FCMS do not possess this ability. For people with FCMS, voluntary movement of cranial musculature is completely absent.

In determining a diagnosis between pseudobulbar palsy, a person must demonstrate whether or not muteness is present, as well as the ability to move the facial, buccal, lingual, and pharyngeal muscles. People with pseudobulbar palsy exhibit, to varying degrees, an ability in these functions, while patients with FCMS do not.

The bilateral form of FCMS ("also known as facio-labio-pharyngo-glosso-laryngo-brachial paralysis)" is consistent with the classic presentation of bilateral corticobulbar involvement. It is characterized by well-preserved automatic and reflex movements. It is caused by lesions in the cortical or subcortical region of the anterior opercular area surrounding the insula forming the gyri of the frontal, temporal, and parietal lobes.

There is some confusion in the terminology used by different neurologists. Mesulam's original description in 1982 of progressive language problems caused by neurodegenerative disease (which he called primary progressive aphasia (PPA) included patients with progressive non-fluent (PNFA), semantic dementia (SD), and logopenic progressive aphasia (LPA).

If a suspected brain injury has occurred, the patient undergoes a series of medical imaging, which could include MRI(magnetic resonance imaging) or CT (computed tomography) scan. After the diagnosis of a brain injury, a speech and language pathologist will perform a variety of tests to determine the classification of aphasia. Additionally, the Boston Assessment of Severe Aphasia (BASA) is a commonly used assessment for diagnosing aphasia. BASA is used to determine treatment plans after strokes lead to symptoms of aphasia and tests both gestural and verbal responses. Cognitive functions can be assessed using the Cognitive Test Battery for Global Aphasia (CoBaGa). The CoBaGa is an appropriate measure to assess a person with severe aphasia because it does not require verbal responses, rather manipulative answers. The CoBaGa assesses cognitive functions such as attention, executive functions, logical reasoning, memory, visual-auditory recognition, and visual-spatial ability. Van Mourik et al. conducted a study in which they assessed the cognitive abilities of people with global aphasia using the Global Aphasic Neuropsychological Battery. This test assesses attention/concentration, memory, intelligence, and visual and auditory nonverbal recognition. The results of this study helped the researchers determine there were varying levels of severity among individuals with global aphasia.

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.

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

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.

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.

This disorder is often associated with brain lesions in the dominant (usually left) hemisphere including the angular and supramarginal gyri (Brodmann area 39 and 40 respectively) near the temporal and parietal lobe junction. There is significant debate in the scientific literature as to whether Gerstmann Syndrome truly represents a unified, theoretically motivated syndrome. Thus its diagnostic utility has been questioned by neurologists and neuropsychologists alike. The angular gyrus is generally involved in translating visual patterns of letter and words into meaningful information, such as is done while reading.

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.

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.

A key deficit in constructional apraxia patients is the inability to correctly copy or draw an image. There are qualitative differences between patients with left hemisphere damage, right hemisphere damage, and Alzheimer's Disease.

The following diagnosis criteria were defined by Mesulam:

- As opposed to having followed trauma to the brain, a patient must show an insidious onset and a gradual progression of aphasia, defined as a disorder of sentence and/or word usage, affecting the production and comprehension of speech.

- The disorder in question must be the only determinant on functional impairment in the activities of the patient’s daily living.

- On the basis of diagnostic procedures, the disorder in question must be unequivocally attributed to a neurodegenerative process.

Whether or not PPA and other aphasias are the only source of cognitive impairment in a patient is often difficult to assess because: 1) as with other neurologically degenerative diseases, such as Alzheimer's disease, there are currently no reliable non-invasive diagnostic tests for aphasias, and thus neuropsychological assessments are the only tool physicians have for diagnosing patients; and 2) aphasias often affect other, non-language portions of these neuropsychological tests, such as those specific for memory.