Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.

Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.

In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli.

Pure alexia, also known as agnosic alexia or alexia without agraphia or pure word blindness, is one form of alexia which makes up "the peripheral dyslexia" group. Individuals who have pure alexia suffer from severe reading problems while other language-related skills such as naming, oral repetition, auditory comprehension or writing are typically intact.

Pure alexia is also known as: "alexia without agraphia", "letter-by-letter dyslexia", "spelling dyslexia", or "word-form dyslexia". Another name for it is "Dejerine syndrome", after Joseph Jules Dejerine, who described it in 1892; however, when using this name, it should not be confused with medial medullary syndrome which shares the same eponym.

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.

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.

Auditory verbal agnosia can be referred to as a pure aphasia because it has a high degree of specificity. Despite an inability to comprehend speech, patients with auditory verbal agnosia typically retain the ability to hear and process non-speech auditory information, speak, read and write. This specificity suggests that there is a separation between speech perception, non-speech auditory processing, and central language processing. In support of this theory, there are cases in which speech and non-speech processing impairments have responded differentially to treatment. For example, some therapies have improved writing comprehension in patients over time, while speech remained critically impaired in those same patients.

The term "pure word deafness" is something of a misnomer. By definition, individuals with pure word deafness are not deaf – in the absence of other impairments, these individuals have normal hearing for all sounds, including speech. The term "deafness" originates from the fact that individuals with AVA are unable to "comprehend" speech that they hear. The term "pure word" refers to the fact that comprehension of verbal information is selectively impaired in AVA. For this reason, AVA is distinct from other auditory agnosias in which the recognition of nonspeech sounds is impaired. Classical (or pure) auditory agnosia is an inability to process environmental sounds. Interpretive or receptive agnosia (amusia) is an inability to understand music.

Patients with pure word deafness complain that speech sounds simply do not register, or that they tend not to come up. Other claims include speech sounding as if it were in a foreign language, the words having a tendency to run together, or the feeling that speech was simply not connected to the patient's voice.

Pure alexia results from cerebral lesions in circumscribed brain regions and therefore belongs to the group of acquired reading disorders, alexia, as opposed to developmental dyslexia found in children who have difficulties in learning to read.

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.

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

Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they do indeed hear sounds being produced, but that the sounds are fundamentally unrecognizable/untranslatable.

1. EXAMINER: What did you eat for breakfast?

2. PATIENT: Breakfast, breakfast, it sounds familiar but it doesn't speak to me. (Obler & Gjerlow 1999:45)

Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman).

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

Agnosias are sensory modality specific, usually classified as visual, auditory, or tactile. Associative visual agnosia refers to a subtype of visual agnosia, which was labeled by Lissauer (1890), as an inability to connect the visual percept (mental representation of something being perceived through the senses) with its related semantic information stored in memory, such as, its name, use, and description. This is distinguished from the visual apperceptive form of visual agnosia, "apperceptive visual agnosia", which is an inability to produce a complete percept, and is associated with a failure in higher order perceptual processing where feature integration is impaired, though individual features can be distinguished. In reality, patients often fall between both distinctions, with some degree of perceptual disturbances exhibited in most cases, and in some cases, patients may be labeled as integrative agnostics when they fit the criteria for both forms. Associative visual agnosias are often category-specific, where recognition of particular categories of items are differentially impaired, which can affect selective classes of stimuli, larger generalized groups or multiple intersecting categories. For example, deficits in recognizing stimuli can be as specific as familiar human faces or as diffuse as living things or non-living things.

An agnosia that affects hearing, "auditory sound agnosia", is broken into subdivisions based on level of processing impaired, and a "semantic-associative" form is investigated within the auditory agnosias.

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.

Associative visual agnosia is a form of visual agnosia. It is an impairment in recognition or assigning meaning to a stimulus that is accurately perceived and not associated with a generalized deficit in intelligence, memory, language or attention. The disorder appears to be very uncommon in a "pure" or uncomplicated form and is usually accompanied by other complex neuropsychological problems due to the nature of the etiology. Afflicted individuals can accurately distinguish the object, as demonstrated by the ability to draw a picture of it or categorize accurately, yet they are unable to identify the object, its features or its functions.

The two main categories of visual agnosia are:

- Apperceptive visual agnosia, impaired object recognition. Individuals with apperceptive visual agnosia cannot form a whole percept of visual information.

- Associative visual agnosia, impaired object identification. Individuals with associative agnosia cannot give a meaning to a formed percept. The percept is created, but it would have no meaning for individuals who have an associative agnosia.

The syndrome rarely presents itself the same way in every patient. Some symptoms that occur may be:

- Constructional apraxia: difficulty in constructing: drawing, copying, designs, copying 3D models

- Topographical disorientation: difficulty finding one's way in the environment

- Optic ataxia: deficit in visually-guided reaching

- Ocular motor apraxia: inability to direct gaze, a breakdown (failure) in starting (initiating) fast eye movements

- Dressing apraxia: difficulty in dressing usually related to inability to orient clothing spatially, and to a disrupted awareness of body parts and the position of the body and its parts in relation to themselves and objects in the environment

- Right-left confusion: difficulty in distinguishing the difference between the directions left and right

There is no uniform performance among patients with auditory verbal agnosia; therefore it is not possible to attribute specific phonetic or phonological deficits to the syndrome. In order to diagnose AVA, two intact abilities need to be established:

- Words that are heard must have undergone adequate acoustic analysis as evidenced by correct repetition;

- The semantic representation of the word must be intact as evidenced by immediate comprehension of the word when presented in written form.

If both of these criteria are met "and" lack of auditory verbal comprehension is apparent, a diagnosis of AVA may follow.

In at least one instance, the Boston Diagnostic Aphasia Examination has been used to profile AVA. This method was able to show that the patient experienced marked difficulty in speech perception with minor to no minor deficits in production, reading, and writing, fitting the profile of AVA. While this provides a well-known example, other verbal-audio test batteries can and have also been used to diagnose pure speech deafness.

Phonological dyslexia is a reading disability that is a form of alexia (acquired dyslexia), resulting from brain injury, stroke, or progressive illness and that affects previously acquired reading abilities. The major distinguishing symptom of acquired phonological dyslexia is that a selective impairment of the ability to read pronounceable non-words occurs although the ability to read familiar words is not affected. It has also been found that the ability to read non-words can be improved if the non-words belong to a family of pseudohomophones.

Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or low intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. There are two types of visual agnosia: apperceptive agnosia and associative agnosia.

Recognition of visual objects occurs at two primary levels. At an apperceptive level, the features of the visual information from the retina are put together to form a perceptual representation of an object. At an associative level, the meaning of an object is attached to the perceptual representation and the object is identified. If a person is unable to recognize objects because they cannot perceive correct forms of the objects, although their knowledge of the objects is intact (i.e. they do not have anomia), they have apperceptive agnosia. If a person correctly perceives the forms and has knowledge of the objects, but cannot identify the objects, they have associative agnosia.

Simultanagnosia (or simultagnosia) is a rare neurological disorder characterized by the inability of an individual to perceive more than a single object at a time. This type of visual attention problem is one of three major components (the others being optic ataxia and optic apraxia) of Bálint's syndrome, an uncommon and incompletely understood variety of severe neuropsychological impairments involving space representation (visuospatial processing). The term "simultanagnosia" was first coined in 1924 by Wolpert to describe a condition where the affected individual could see individual details of a complex scene but failed to grasp the overall meaning of the image.

Simultanagnosia can be divided into two different categories: dorsal and ventral. Ventral occipito-temporal lesions cause a mild form of the disorder, while dorsal occipito-parietal lesions cause a more severe form of the disorder.

Patients with simultanagnosia, a component of Bálint's syndrome, have a restricted spatial window of visual attention and cannot see more than one object at a time in a scene that contains more than one object. For instance, if presented with an image of a table containing both food and various utensils, a patient will report seeing only one item, such as a spoon. If the patient's attention is redirected to another object in the scene, such as a glass, the patient will report that they see the glass but no longer see the spoon. As a result of this impairment, simultanagnosic patients often fail to comprehend the overall meaning of a scene.

In addition, patients note that one stationary object may spontaneously disappear from view as they become aware of another object in the scene.

Simultanagnosic patients often exhibit a phenomenon known as "local capture" where they only identify the local elements of stimuli containing local and global features. However, recent studies have demonstrated that implicit processing of the global structure can occur. With the appropriate stimulus conditions, explicit processing of the global form may occur. For example, a study performed with Navon hierarchical letters, which are large letters composed of smaller ones, revealed that the use of smaller and denser Navon letters biased the patient towards global processing.

Visuospatial dysgnosia is a loss of the sense of "whereness" in the relation of oneself to one's environment and in the relation of objects to each other. Visuospatial dysgnosia is often linked with topographical disorientation.

Patients with autotopagnosia exhibit an inability to locate parts of their own body, the body of an examiner’s, or the parts of a representation of a human body. Deficiencies can be in localizing parts of a certain area of the body, or the entire body.

Some patients demonstrating the symptoms of autotopagnosia have a decreased ability to locate parts of other multipart object. Patients are considered to suffer from “pure” autotopagnosia, however, if their deficiency is specific to body part localization. Patients suffering from “pure” autotopagnosia often have no problems carrying out tasks involved in everyday life that require body part awareness. Patients have difficulty locating body parts when directly asked, but can carry out activities such as putting on pants without difficulty. Patients can describe the function and appearance of body parts, yet they are still unable to locate them.

Damage to the left parietal lobe can result in what is called Gerstmann syndrome. It can include right-left confusion, a difficulty with writing Agraphia and a difficulty with mathematics Acalculia. In addition, it can also produce language deficiencies Aphasia and an inability to recognize objects normally Agnosia.

Other related disorders include:

- Apraxia: an inability to perform skilled movements despite understanding of the movements and intact sensory and motor systems.

- Finger agnosia: An inability to name the fingers, move a specific finger upon being asked, and/or recognize which finger has been touched when an examiner touches one.

Autotopagnosia from the Greek "a" and "gnosis," meaning "without knowledge", "topos" meaning "place", and "auto" meaning "oneself", autotopagnosia virtually translates to the "lack of knowledge about one's own space," and is clinically described as such.

Autotopagnosia is a form of agnosia, characterized by an inability to localize and orient different parts of the body. The psychoneurological disorder has also been referred to as "body-image agnosia" or "somatotopagnosia." "Somatotopagnosia" has been argued to be a better suited term to describe the condition. While autotopagnosia emphasizes the deficiencies in localizing only one's own body parts and orientation, "somatotopagnosia" also considers the inability to orient and recognize the body parts of others or representations of the body (e.g., manikins, diagrams).

Typically, the cause of autotopagnosia is a lesion found in the parietal lobe of the left hemisphere of the brain. However, it as also been noted that patients with generalized brain damage present with similar symptoms of autotopagnosia.

As a concept, autotopagnosia has been criticized as nonspecific; some claim that this is a manifestation of a greater symptomatic complex of anomia, marked by an inability to name things in general—not just parts of the human body.

Semantic dyslexia is, as the name suggests, a subtype of the group of cognitive disorders known as alexia (acquired dyslexia). Those who suffer from semantic dyslexia are unable to properly attach words to their meanings in reading and/or speech. When confronted with the word "diamond", they may understand it as "sapphire", "shiny" or "diamonds"; when asking for a bus ticket, they may ask for some paper or simply "a thing".

Semantic dementia (SD) is a degenerative disease characterized by atrophy of anterior temporal regions (the primary auditory cortex; process auditory information) and progressive loss of semantic memory. SD patients often present with surface dyslexia, a relatively selective impairment in reading low-frequency words with exceptional or atypical spelling-to-sound correspondences.

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.