The Landau–Kleffner syndrome is characterized by the sudden or gradual development of aphasia (the inability to understand or express language) and an abnormal electroencephalogram (EEG). LKS affects the parts of the brain that control comprehension and speech (Broca's area and Wernicke's area). The disorder usually occurs in children between the ages of 3 and 7 years. There appears to be a male dominance in the diagnosis of the syndrome (ratio of 1.7:1, men to women).

Typically, children with LKS develop normally, but then lose their language skills. While many affected individuals have clinical seizures, some only have electrographic seizures, including electrographic status epilepticus of sleep (ESES). The first indication of the language problem is usually auditory verbal agnosia. This is demonstrated in patients in multiple ways including the inability to recognize familiar noises and the impairment of the ability to lateralize or localize sound. In addition, receptive language is often critically impaired, however in some patients, impairment in expressive language is the most profound. In a study of 77 cases of Landau–Kleffner syndrome, 6 were found to have this type of aphasia. Because this syndrome appears during such a critical period of language acquisition in a child's life, speech production may be affected just as severely as language comprehension. The onset of LKS is typically between 18 months and 13 years, the most predominant time of emergence being between 3 and 7 years.

Generally, earlier manifestation of the disease correlates with poorer language recovery, and with the appearance of night seizures that last for longer than 36 months. LKS has a wide range of symptom differences and lacks a uniformity in diagnostic criteria between cases, and many studies don't include follow-ups on the patients, so no other relationships between symptoms and recovery have been made known.

Language deterioration in patients typically occurs over a period of weeks or months. However, acute onset of the condition has also been reported as well as episodic aphasia.

Seizures, especially during the night, are a heavily weighted indicator of LKS. The prevalence of clinical seizures in acquired epileptic aphasia (LKS) is 70-85%. In one third of patients, only a single episode of a seizure was recorded. The seizures typically appear between the ages of 4 and 10 and disappear before adulthood (around the age of 15).

Often, behavioral and neuropsychologic disturbances accompany the progression of LKS. Behavioral issues are seen in as many as 78% of all cases. Hyperactivity and a decreased attention span are observed in as many as 80% of patients as well as rage, aggression, and anxiety. These behavior patterns are considered secondary to the language impairment in LKS. Impaired short-term memory is a feature recorded in long-standing cases of acquired epileptic aphasia.

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

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.

Landau–Kleffner syndrome (LKS)—also called infantile acquired aphasia, acquired epileptic aphasia or aphasia with convulsive disorder—is a rare childhood neurological syndrome.

It is named after William Landau and Frank Kleffner, who characterized it in 1957 with a diagnosis of six children.

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.

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 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.

Given the previously stated signs and symptoms the following behaviors are often seen in people with aphasia as a result of attempted compensation for incurred speech and language deficits:

- Self-repairs: Further disruptions in fluent speech as a result of mis-attempts to repair erred speech production.

- Speech disfluencies: Include previously mentioned disfluencies including repetitions and prolongations at the phonemic, syllable and word level presenting in pathological/ severe levels of frequency.

- Struggle in non-fluent aphasias: A severe increase in expelled effort to speak after a life where talking and communicating was an ability that came so easily can cause visible frustration.

- Preserved and automatic language: A behavior in which some language or language sequences that were used so frequently, prior to onset, they still possess the ability to produce them with more ease than other language post onset.

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.

The following are common symptoms seen in patients with Wernicke's aphasia:

Impaired Comprehension: deficits in understanding (receptive) written and spoken language. This is because Wernicke's area is responsible for assigning meaning to the language that is heard, so if it is damaged, the brain cannot comprehend the information that is being received.

Poor Word Retrieval: ability to retrieve target words is impaired. This is also referred to as Anomia.

Fluent Speech: individuals with Wernicke's aphasia do not have difficulty with producing connected speech that flows.. Although the connection of the words may be appropriate, the words they are using may not belong together or make sense (see Production of Jargon below).

Production of Jargon: speech that lacks content, consists of typical intonation, and is structurally intact. Jargon can consist of a string of neologisms, as well as a combination of real words that do not make sense together in context.

Awareness: Individuals with Wernicke's aphasia are often not aware of their incorrect productions, which would further explain why they do not correct themselves when they produce jargon, paraphasias, or neologisms.

Paraphasias:

- Phonemic (Literal) Paraphasias: involves the substitution, addition, or rearrangement of sounds so that an error can be defined as sounding like the target word. Often, half of the word is still intact which allows for easy comparison to the appropriate, original word.

- Ex: "bap" for "map"

- Semantic (Verbal) Paraphasias: saying a word that is related to the target word in meaning or category; frequently observed in Wernicke's aphasia.

- Ex: "jet" for "airplane" or "knife" for "fork"

Neologisms: nonwords that have no relation to the target word.

- Ex: "dorflur" for "shoe"

Circumlocution: talking around the target word.

- Ex: "uhhh it's white...it's flat...you write on it…" (when referencing paper)

Press of speech: run-on speech.

- If a clinician asks, "what do you do at a supermarket?" And the individual responds with "Well, the supermarket is a place. It is a place with a lot of food. My favorite food is italian food. At a supermarket, I buy different kinds of food. There are carts and baskets. Supermarkets have lots of customers, and workers…."

Lack of Hemiparesis: typically, no motor deficits are seen with a localized lesion in Wernicke's area.

Reduced Retention Span: reduced ability to retain information for extended periods of time.

Impairments in reading and writing: impairments can be seen in both reading and writing with differing severity levels.

How to Differentiate from Other Types of Aphasia.

- Expressive Aphasia (non-fluent Broca's Aphasia): individuals have great difficulty forming complete sentences with generally only basic content words (leaving out words like "is" and "the").

- Global Aphasia: individuals have extreme difficulties with both expressive (producing language) and receptive (understanding language).

- Anomic Aphasia: the biggest hallmark is an individuals poor word finding abilities; their speech is fluent and appropriate, but full of circumlocutions (evident in both writing and speech).

- Conduction Aphasia: individual can comprehend what is being said and is fluent in spontaneous speech, but they cannot repeat what is being said to them.

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.

Conduction aphasics will show relatively well-preserved auditory comprehension, which may even be completely functional. Spontaneous speech production will be fluent and generally grammatically and syntactically correct. Intonation and articulation will also be preserved. Speech will often contain paraphasic errors: phonemes and syllables will be dropped or transposed (e.g., "snowball" → "snowall", "television" → "vellitision", "ninety-five percent" → "ninety-twenty percent"). The hallmark deficit of this disorder, however, is in repetition. Patients will show a marked inability to repeat words or sentences when prompted by an examiner. After saying a sentence to a person with conduction aphasia, he or she will be able to paraphrase the sentence accurately but will not be able to repeat it, possibly because their "motor speech error processing is disrupted by inaccurate forward predictions, or because detected errors are not translated into corrective commands due to damage to the auditory-motor interface". When prompted to repeat words, patients will be unable to do so, and produce many paraphasic errors. For example, when prompted with "bagger", a patient may respond with, "gabber". Oral reading can also be poor.

However, patients recognize their paraphasias and errors and will try to correct them, with multiple attempts often necessary for success. This recognition is due to preserved auditory error detection mechanisms. Error sequences frequently fit a pattern of incorrect approximations featuring known morphemes that "a") share one or more similarly located phonemes but "b") differ in at least one aspect that makes the substituted morpheme(s) semantically distinct. This repetitive effort to approximate the appropriate word or phrase is known as "conduite d’approche". For example, when prompted to repeat "Rosenkranz", a German-speaking patient may respond with, "rosenbrau... rosenbrauch... rosengrau... bro... grosenbrau... grossenlau, rosenkranz... kranz... rosenkranz".

Conduction aphasia is a relatively mild language impairment, and most patients return to day-to-day life. Symptoms of conduction aphasia, as with other aphasias, can be transient, lasting only several hours or a few days. As aphasias and other language disorders are frequently due to stroke, their symptoms can change and evolve over time, or simply disappear. This is due to healing in the brain after inflammation or hemorrhage, which leads to decreased local impairment. Furthermore, plastic changes in the brain may lead to the recruitment of new pathways to restore lost function. For example, the right hemisphere speech systems may learn to correct for left-hemisphere damage. However, chronic conduction aphasia is possible, without transformation to other aphasias. These patients show prolonged, profound deficits in repetition, frequent phonemic paraphasias, and "conduite d'approche" during spontaneous speech.

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).

Three classifications of primary progressive aphasia have been described. In the classical Mesulam criteria for primary progressive aphasia, there are two variants: a non-fluent type progressive nonfluent aphasia (PNFA) and a fluent type semantic dementia (SD). A third variant of primary progressive aphasia, logopenic progressive aphasia (LPA), is an atypical form of Alzheimer's disease. Early PNFA can include such features as speech apraxia, effortful speech, and anomia, and thus can resemble Broca’s aphasia. Early LPA involves impairments in naming and sentence repetition, and thus can resemble Conduction aphasia. However, these PPA subtypes differ from these similar aphasias, as these subtypes do not occur acutely following trauma to the brain, such as following a stroke, due to differing functional and structural neuroanatomical patterns of involvement and the progressive nature of the disease.

Transcortical motor aphasia (TMoA), also known as commissural dysphasia or white matter dysphasia, results from damage in the anterior superior frontal lobe of the language-dominant hemisphere. This damage is typically due to cerebrovascular accident (CVA). TMoA is generally characterized by reduced speech output, which is a result of dysfunction of the affected region of the brain. The left hemisphere is usually responsible for performing language functions, although left-handed individuals have been shown to perform language functions using either their left or right hemisphere depending on the individual. The anterior frontal lobes of the language-dominant hemisphere are essential for initiating and maintaining speech. Because of this, individuals with TMoA often present with difficulty in speech maintenance and initiation.

Damage in the watershed region does not directly harm the areas of the brain involved in language production or comprehension; instead, the damage isolates these areas from the rest of the brain. If there is damage to the frontal lobe, executive functions related to language use are often affected. Executive functions relevant to language include activating language responses, controlling syntax (grammar), and narrative discourse. Difficulties in these areas can lead to supplementary deficits involving difficulties forming complex sentences, choosing which words to use appropriately, and initiating speech in conversation.

The extent and location of the brain damage will impact the degree and variety of language functioning characteristics (i.e. damage deep to the frontal lobe and/or damage across multiple regions will greatly impair language). Right hemiparesis, or right-sided paralysis, may coincide with TMoA if the lesion in the anterior frontal lobe is large enough and extends into the posterior frontal lobe.

There are some other forms of aphasia that relate to TMoA. For instance, adynamic aphasia is a form of TMoA that is characterized by sparse speech. This occurs as a result of executive functioning in the frontal lobe. Another form of aphasia related to TMoA is dynamic aphasia. Patients with this form of aphasia may present with a contiguity disorder in which they have difficulty combining linguistic elements. For dynamic aphasia, this is most apparent when the patient is asked to sequence at the sentence level whereas for other aphasias contiguity disorder can be seen at the phoneme or word level.

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia will try to hide their inability to name objects by using words like "thing". So when asked to name a pencil they may say it is a thing used to write.

- Inability to comprehend language

- Inability to pronounce, not due to muscle paralysis or weakness

- Inability to speak spontaneously

- Inability to form words

- Inability to name objects (anomia)

- Poor enunciation

- Excessive creation and use of personal neologisms

- Inability to repeat a phrase

- Persistent repetition of one syllable, word, or phrase (stereotypies)

- Paraphasia (substituting letters, syllables or words)

- Agrammatism (inability to speak in a grammatically correct fashion)

- Dysprosody (alterations in inflexion, stress, and rhythm)

- Incomplete sentences

- Inability to read

- Inability to write

- Limited verbal output

- Difficulty in naming

- Speech disorder

- Speaking gibberish

- Inability to follow or understand simple requests

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.

Disconnection syndrome is a general term for a number of neurological symptoms caused by damage to the white matter axons of communication pathways—via lesions to association fibers or commissural fibers—in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

Callosal syndrome, or split-brain, is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms. Other types of disconnection syndrome include conduction aphasia (lesion of the association tract connecting Broca’s area and Wernicke’s), agnosia, apraxia, pure alexia, etc.

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.

Paraphasia is associated with fluent aphasias, characterized by “fluent spontaneous speech, long grammatically shaped sentences and preserved prosody abilities.” Examples of these fluent aphasias include receptive or Wernicke’s aphasia, anomic aphasia, conduction aphasia, and transcortical sensory aphasia, among others. All of these lead to a difference in processing efficiency, which is often caused by damage to a cortical region in the brain (in receptive aphasia, for example, the lesion is in or near Wernicke’s area); lesion location is the most important determining factor for all aphasic disorders, including paraphasia - the location of the lesion can be used to hypothesize the type of aphasic symptoms the patient will display. This lesion can be caused by a variety of different methods: malfunctioning blood vessels (caused, for example, by a stroke) in the brain are the cause of 80% of aphasias in adults, as compared to head injuries, dementia and degenerative diseases, poisoning, metabolic disorders, infectious diseases, and demyelinating diseases. Lesions involving the posterior superior temporal lobe are often associated with fluent aphasias.

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").

Paraphasia is a type of language output error commonly associated with aphasia, and characterized by the production of unintended syllables, words, or phrases during the effort to speak. Paraphasic errors are most common in patients with fluent forms of aphasia, and comes in three forms: phonemic or literal, neologistic, and verbal. Paraphasias can affect metrical information, segmental information, number of syllables, or both. Some paraphasias preserve the meter without segmentation, and some do the opposite. However, most paraphasias affect both partially.

The term was apparently introduced in 1877 by the German-English physician Julius Althaus in his book on "Diseases of the Nervous System", in a sentence reading, "In some cases there is a perfect chorea or delirium of words, which may be called "paraphasia"".