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.

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.

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.

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.

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.

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 (AVA), also known as pure word deafness, is the inability to comprehend speech. Individuals with this disorder lose the ability to understand language, repeat words, and write from dictation. Some patients with AVA describe hearing spoken language as meaningless noise, often as though the person speaking was doing so in a foreign language. However, spontaneous speaking, reading, and writing are preserved. The maintenance of the ability to process non-speech auditory information, including music, also remains relatively more intact than spoken language comprehension. Individuals who exhibit pure word deafness are also still able to recognize non-verbal sounds. The ability to interpret language via lip reading, hand gestures, and context clues is preserved as well. Sometimes, this agnosia is preceded by cortical deafness; however, this is not always the case. Researchers have documented that in most patients exhibiting auditory verbal agnosia, the discrimination of consonants is more difficult than that of vowels, but as with most neurological disorders, there is variation among patients.

Auditory verbal agnosia (AVA) is not the same as Auditory agnosia; patients with (nonverbal) auditory agnosia have a relatively more intact speech comprehension system despite their impaired recognition of nonspeech sounds.

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).

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.

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.

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 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.

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.

Transcortical sensory aphasia is caused by lesions in the inferior left temporal lobe of the brain located near Wernicke's area, and is usually due to minor hemorrhage or contusion in the temporal lobe, or infarcts of the left posterior cerebral artery (PCA). One function of the arcuate fasciculus is the connection between Wernicke’s and Broca’s area. In TSA Wernicke’s and Broca’s areas are spared, meaning that lesions do not occur in these regions of the brain. However, since the arcuate fasciculus, Wernicke's area, and Broca's area are secluded from the rest of the brain in TSA, patients still have intact repetition (as information from the arcuate fasciculus is relayed to Broca’s area), but cannot attach meaning to words, either spoken or heard.

Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but a neurological inability of the brain to process sound meaning. It is a disruption of the "what" pathway in the brain. Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it "was" a lion creating the noise. Auditory agnosia is caused by damage to the secondary and tertiary auditory cortex of the temporal lobe of the brain.

Apperceptive agnosia is a failure in recognition that is due to a failure of perception. In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur. When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; This occurs because apperceptive agnosia is most likely to present visual impairments. However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas.

Symptoms generally include memory or learning impairments, with the inability to integrate parts coherently.There is a big range to the severity of this disease and often the symptoms that are shown in each patient vary as well. As ambiguous as the general symptoms may be, patients are often treated of their respective symptoms as they appear and how critical the conditions are.

There are three primary distinctions of auditory agnosia that fall into two categories.

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.

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.

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.

Integrative agnosia is a sub-disease of agnosia, meaning the lack of integrating perceptual wholes within

knowledge. Integrative agnosia can be assessed by several experimental tests such as the Efron shape test, which

determines the specificity of the disease being Integrative.

This disease is often caused by brain trauma, producing medial ventral lesions to the extrastriate cortex. Affecting this region of the brain produces learning impairments: the inability to

integrate parts such as spatial distances or producing visual images from short or long-term memory.

Prosopagnosia, also called face blindness, is a cognitive disorder of face perception in which the ability to recognize familiar faces, including one's own face (self-recognition), is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact. The term originally referred to a condition following acute brain damage (acquired prosopagnosia), but a congenital or developmental form of the disorder also exists, which may affect up to 2.5% of the United States population. The specific brain area usually associated with prosopagnosia is the fusiform gyrus, which activates specifically in response to faces. The functionality of the fusiform gyrus allows most people to recognize faces in more detail than they do similarly complex inanimate objects. For those with prosopagnosia, the new method for recognizing faces depends on the less-sensitive object recognition system. The right hemisphere fusiform gyrus is more often involved in familiar face recognition than the left. It remains unclear whether the fusiform gyrus is only specific for the recognition of human faces or if it is also involved in highly trained visual stimuli.

There are two types of prosopagnosia: acquired and congenital (developmental). Acquired prosopagnosia results from occipito-temporal lobe damage and is most often found in adults. This is further subdivided into apperceptive and associative prosopagnosia. In congenital prosopagnosia, the individual never adequately develops the ability to recognize faces.

Though there have been several attempts at remediation, no therapies have demonstrated lasting real-world improvements across a group of prosopagnosics. Prosopagnosics often learn to use "piecemeal" or "feature-by-feature" recognition strategies. This may involve secondary clues such as clothing, gait, hair color, skin color, body shape, and voice. Because the face seems to function as an important identifying feature in memory, it can also be difficult for people with this condition to keep track of information about people, and socialize normally with others. Prosopagnosia has also been associated with other disorders that are associated with nearby brain areas: left hemianopsia (loss of vision from left side of space, associated with damage to the right occipital lobe), achromatopsia (a deficit in color perception often associated with unilateral or bilateral lesions in the temporo-occipital junction) and topographical disorientation (a loss of environmental familiarity and difficulties in using landmarks, associated with lesions in the posterior part of the parahippocampal gyrus and anterior part of the lingual gyrus of the right hemisphere). It is from the Greek: "prosopon" = "face" and "agnosia" = "not knowing".

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