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.

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.

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.

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.

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 severity of the type of aphasia varies depending on the size of the stroke. However, there is much variance between how often one type of severity occurs in certain types of aphasia. For instance, any type of aphasia can range from mild to profound. Regardless of the severity of aphasia, people can make improvements due to spontaneous recovery and treatment in the acute stages of recovery. Klebic et al. (2011) found that people with severe aphasia improved after receiving therapy for a year, consequently reducing the severity of their aphasia. Additionally, while most studies propose that the greatest outcomes occur in people with severe aphasia when treatment is provided in the acute stages of recovery, Robey (1998) also found that those with severe aphasia are capable of making strong language gains in the chronic stage of recovery as well. This finding implies that persons with aphasia have the potential to have functional outcomes regardless of how severe their aphasia may be. While there is no distinct pattern of the outcomes of aphasia based on severity alone, global aphasia typically make functional language gains, but may be gradual since global aphasia affects many language areas.

Logopenic progressive aphasia (LPA) is a form of primary progressive aphasia. It is defined clinically by impairments in naming and sentence repetition. It is similar to conduction aphasia and is associated with atrophy to the left posterior temporal cortex and inferior parietal lobule. It is suspected that an atypical form of Alzheimer's disease is the most common cause of logopenic progressive aphasia.

Although patients with the logopenic variant of PPA are still able to produce speech, their speech rate may be significantly slowed down due to word retrieval difficulty. Over time, they may experience the inability to retain lengthy information, causing problems with understanding complex verbal information. Some additional behavioral features include irritability, anxiety and agitation.

Compared to other forms of primary progressive aphasia, the logopenic variant has been found to be associated with cognitive and behavioral characteristics. Studies have shown that patients with the logopenic variant perform significantly worse on tests of calculation than other primary progressive aphasia patients. Several logopenic variant patients, especially those with Alzheimer’s disease pathology, have also been found to perform poorly on memory tasks.

Logopenic progressive aphasia is caused by damage to segregated brain regions, specifically the inferior parietal lobe and superior temporal regions. Difficulties in naming are produced from the thinning of the inferior parietal lobe. Damage to the dorsal pathways creates language deficiency in patients that is characteristic of logopenic progressive aphasia.

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.

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.

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.

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.

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.

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

There are three main types of anomia:

- Word selection anomia occurs when the patient knows how to use an object and can correctly select the target object from a group of objects, and yet cannot name the object. Some patients with word selection anomia may exhibit selective impairment in naming particular types of objects, such as animals or colors. In the subtype known as color anomia, the patient can distinguish between colors but cannot identify them by name or name the color of an object. The patients can separate colors into categories, but they cannot name them.

- Semantic anomia is a disorder in which the meaning of words becomes lost. In patients with semantic anomia, a naming deficit is accompanied by a recognition deficit. Thus, unlike patients with word selection anomia, patients with semantic anomia are unable to select the correct object from a group of objects, even when provided with the name of the target object.

- Disconnection anomia results from the severing of connections between sensory and language cortices. Patients with disconnection anomia may exhibit modality-specific anomia, where the anomia is limited to a specific sensory modality, such as hearing. For example, a patient who is perfectly capable of naming a target object when it is presented via certain sensory modalities like audition or touch, may be unable to name the same object when the object is presented visually. Thus, in such a case, the patient's anomia arises as a consequence of a disconnect between his/her visual cortex and language cortices.

Asemia is a more severe condition than aphasia, so it does have some similarities with the disease. People who have asemia have the inability to comprehend signs, symbols, and even language. They also have the inability to use signs, symbols, and language. People with asemia sometimes may take up asemic writing, which is "wordless" writing. What wordless writing could mean is that the writing looks like regular or traditional writing, but there is no content that makes sense. The concept of syntax, semantics, or even communication does not exist in asemic writing.

Semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain (with loss of word meaning). SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD), with the other two being frontotemporal dementia and progressive nonfluent aphasia. SD is a clinically defined syndrome, but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). SD is one of the three variants of Primary Progressive Aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease. It is important to note the distinctions between Alzheimer’s Disease and Semantic dementia with regard to types of memory affected. In general, Alzheimer’s Disease is referred to as disorder affecting mainly episodic memory, defined as the memory related to specific, personal events distinct for each individual. Semantic dementia generally affects semantic memory, which refers to long-term memory that deals with common knowledge and facts.3

It was first described by Arnold Pick in 1904 and in modern times was characterized by Professor Elizabeth Warrington in 1975, but it was not given the name semantic dementia until 1989. The clinical and neuropsychological features, and their association with temporal lobe atrophy were described by Professor John Hodges and colleagues in 1992.

Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernicke's aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities, and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits (i.e. hemiparesis) do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Wernicke's aphasia was named after Carl Wernicke who is credited with discovering the area of the brain responsible for language comprehension. Individuals with Wernicke's aphasia are typically unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.

Like many acquired language disorders, Wernicke's aphasia can be experienced in many different ways and to many different degrees. Patients diagnosed with Wernicke's aphasia can show severe language comprehension deficits; however, this is dependent on the severity and extent of the lesion. Severity levels may range from being unable to understand even the simplest spoken and/or written information to missing minor details of a conversation. Many diagnosed with Wernicke's aphasia have difficulty with repetition in words and sentences, and or working memory.

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.

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.

Asemia is the term for the medical condition of being unable to understand or express any signs or symbols.

It is a more severe condition than aphasia, which is the inability to understand linguistic signs. Asemia is caused by damage to the areas of the brain that process communication – more specifically, when there is damage to the left side of the brain in the areas that process communication such as Broca's and Wernicke's areas. Damage can be inflicted by physical trauma to the brain, but is more commonly caused by stroke and sometimes tumors. The onset of this condition is usually quick but not permanent. Treatment of this condition is traditional speech therapy in which the individual must relearn how to read, write, and talk. Depending on the severity of the injury, recovery can take days to years. Considerable recovery is common, but often not to the full extent of baseline ability.

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

In all of these ways, TSA is very similar to a more commonly known language disorder, receptive aphasia. However, transcortical sensory aphasia differs from receptive aphasia in that patients still have intact repetition and exhibit echolalia, or the compulsive repetition of words. Transcortical sensory aphasia cannot be diagnosed through brain imaging techniques such as functional magnetic resonance imaging (fMRI), as the results are often difficult to interpret. Therefore, clinicians rely on language assessments and observations to determine if a patient presents with the characteristics of TSA. Patients diagnosed with TSA have shown partial recovery of speech and comprehension after beginning speech therapy. Speech therapy methods for patients with any subtype of aphasia are based on the principles of learning and neuroplasticity. Clinical research on TSA is limited because it occurs so infrequently in patients with aphasia that it is very difficult to perform systematic studies.

TSA should not be confused with transcortical motor aphasia (TMA), which is characterized by nonfluent speech output, with good comprehension and repetition. Patients with TMA have impaired writing skills, difficulty speaking and difficulty maintaining a clear thought process. Furthermore, TMA is caused by lesions in cortical motor areas of the brain as well as lesions in the anterior portion of the basal ganglia, and can be seen in patients with expressive aphasia.

Aphasia is loss of the ability to produce or comprehend language. There are acute aphasias which result from stroke or brain injury, and primary progressive aphasias caused by progressive illnesses such as dementia.

- Acute aphasias

- Expressive aphasia also known as Broca's aphasia, expressive aphasia is a non-fluent aphasia that is characterized by damage to the frontal lobe region of the brain. A person with expressive aphasia usually speaks in short sentences that make sense but take great effort to produce. Also, a person with expressive aphasia understands another person's speech but has trouble responding quickly.

- Receptive aphasia also known as Wernicke's aphasia, receptive aphasia is a fluent aphasia that is categorized by damage to the temporal lobe region of the brain. A person with receptive aphasia usually speaks in long sentences that have no meaning or content. People with this type of aphasia often have trouble understanding other's speech and generally do not realize that they are not making any sense.

- Conduction aphasia

- Anomic aphasia

- Global aphasia

- Primary progressive aphasias

- Progressive nonfluent aphasia

- Semantic dementia

- Logopenic progressive aphasia

Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia. An acquired language disorder, it is characterized by intact auditory comprehension, fluent (yet paraphasic) speech production, but poor speech repetition. They are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as patients show significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. Patients will display frequent errors during spontaneous speech, such as substituting or transposing sounds. They will also be aware of their errors, and will show significant difficulty correcting them. For example: "Clinician: Now, I want you to say some words after me. Say ‘boy’. Patient: Boy. Clinician: Home. Patient: Home. Clinician: Seventy-nine. Patient: Ninety-seven. No … sevinty-sine … siventy-nice…. Clinician: Let’s try another one. Say ‘refrigerator’. Patient: Frigilator … no? how about … frerigilator … no frigaliterlater … aahh! It’s all mixed up!"

Shallice and Warrington (1970) were able to differentiate two variants of

this constellation: the reproduction and the repetition type. These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, afflicting confrontation tasks such as repetition, reading and naming in a similar manner.

Left-hemisphere damage involving auditory regions often result in speech deficits. Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech. Studies have suggested that conduction aphasia is a result of damage specifically to the left superior temporal gyrus and/or the left supra marginal gyrus. The classical explanation for conduction aphasia is that of a disconnection between the brain areas responsible for speech comprehension (Wernicke's area) and speech production (Broca's area), due specifically to damage to the arcuate fasciculus, a deep white matter tract. Patients are still able to comprehend speech because the lesion does not disrupt the ventral stream pathway.