Agnosia

Last updated
Agnosia
Nuvola apps interrogation blue.png
Agnosia causes loss of the ability to recognize or comprehend the meaning of objects even with intact senses.
Specialty Psychiatry, Neurology, Neuropsychology
Picture of the ventral and dorsal streams. The ventral stream is depicted in purple and the dorsal stream is depicted in green. Ventral-dorsal streams.svg
Picture of the ventral and dorsal streams. The ventral stream is depicted in purple and the dorsal stream is depicted in green.

Agnosia is a neurological disorder characterized by an inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. [1] It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. [2] Agnosia only affects a single modality, [3] such as vision or hearing. [4] More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information. [5]

Contents

Types

NameDescription
Akinetopsia Also known as cerebral akinetopsia, this is associated with the inability to see visual motion. One cause of cerebral akinetopsia is lesions outside the striate cortex. [6]
AllotopagnosiaPatients cannot point at external targets located outside their own body, whether other persons' body parts or objects, but they perfectly point at their own body parts.
Anosognosia This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive visual agnosia Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients with associative agnosia, those with apperceptive agnosia are unable to copy images. [7]
Associative visual agnosia Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients with associative agnosia are still able to reproduce an image through copying.
Astereognosis Also known as somatosensory agnosia, it is connected to tactile sense—that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Auditory agnosia Auditory agnosia has been recognized since 1877. [8] With auditory agnosia, there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal. There are two types of auditory agnosia: semantic associative and discriminative agnosia. Semantic associative agnosia is associated with lesions to the left hemisphere, whereas discriminative agnosia is associated with lesions to the right hemisphere. [9]
Auditory verbal agnosia Also known as pure word deafness (PWD). This presents as a form of meaning "deafness" in which hearing is intact but there is significant difficulty recognising spoken words as semantically meaningful.
Autotopagnosia Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Cerebral achromatopsia A difficulty in perceiving colors in which the world may appear drab or in shades of gray. Cerebral achromatopsia is caused by neurological damage. [10] [11] There are two regions of the brain which specialize for color recognition, areas V4 and V8. If there is a unilateral lesion to area V4, a loss of color perception in only half of the visual field may result known as hemiachromatopsia. [3] Similar, but distinct, is color agnosia, which involves having difficulty recognizing colors, while still being able to perceive them as measured by a color matching or categorizing task. [12]
Cortical deafness Refers to people who do not perceive any auditory information but whose hearing is intact.
Environmental agnosiaIt is the inability to locate a specific room or building that one is familiar with, as well as the inability to provide directions for how to arrive at a particular location. These individuals experience difficulty with learning routes. This form of agnosia is often associated with lesions to the bilateral or right hemisphere posterior regions. It is also associated with prosopagnosia and Parkinson's disease. [3]
Finger agnosia Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form agnosiaPatients perceive only parts of details, not the whole object.
Heterotopagnosia Patients cannot point at another person's body parts, but can point at their own body parts.
Integrative agnosia Usually a patient has a form of associative agnosia or apperceptive agnosia. However, in the case of integrative agnosia a patient falls in between a form of associative and apperceptive agnosia. This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Pain agnosiaAlso referred to as congenital analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia Is the inability to recognize familiar voices, even though the hearer can understand the words used. [13]
Prosopagnosia Also known as faceblindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Pure alexia Inability to recognize text. Patients with pure alexia often have damage to their corpus callosum, as well as damage to the left visual association areas. [3] Pure alexia involves not being able to read printed material, but these individuals still have the ability to write. Individuals with pure alexia usually read words letter by letter. [14] However, individuals with pure alexia show a frequency effect. They are able to read high frequency words better and faster than they can read low frequency words. [15]
Semantic agnosiaThose with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognise the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realisation of its semantics (meaning). [16]
Social-emotional agnosia Sometimes referred to as expressive agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Simultagnosia The inability to process visual input as a whole. The person instead processes faces, bodies, objects, rooms, places, pictures in a bit-by-bit fashion. [17] When looking at a picture they can describe the parts of the picture but struggle to comprehend the picture as a whole. Simultagnosia occurs in Bálint syndrome [18] but may also occur in brain injury. This condition can also be described by only seeing one object at a time. An example is having two cups in your visual field and only being able to see one at a time.
Tactile agnosia Impaired ability to recognize or identify objects by touch alone. [19]
Topographical disorientation Also known as topographical agnosia or topographagnosia, this is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognize objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place. Patients with topographical agnosia have the ability to read maps, but become lost in familiar environments. [20]
Visuospatial dysgnosia This 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. It may include constructional apraxia, topographical disorientation, optic ataxia, ocular motor apraxia, dressing apraxia, and right-left confusion.[ citation needed ]
Visual agnosia Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects. [21]

Visual agnosia

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. [22]

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. [22]

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. [22] 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. [22] However, individuals with prosopagnosia can recognize all other types of visual stimuli. [23]

Speech agnosia

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 hear sounds being produced, but that the sounds are fundamentally unrecognizable or untranslatable. [24]

  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). [24]

Causes

Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. [4] Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved. [4]

Patients who experience dramatic recovery from blindness experience significant to total agnosia. [25]

The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). [24] For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface:

The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it is understood today, speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex. [24]

Diagnosis

In order to assess an individual for agnosia, it must be verified that the individual does not have a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual has a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual has a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed. [3]

Pure alexia

Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters. [3]

Prosopagnosia

Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age and culture appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture. [3]

Treatment

For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.[ citation needed ]

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies. [3]

Verbal strategies

Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues. [3]

Alternate cues

Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate visual cues such as a scar on an individual's face or crooked teeth, or cues from other senses, like the sound of an individual's voice, in order to recognize the individual. [3] Hair color and length can be helpful cues as well. [5]

Organizational strategies

Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues. [3]

Current research

There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. [4] Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials. [26]

History

The term "agnosia" comes from the Ancient Greek ἀγνωσία (agnosia), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: [27] "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'." Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech. [8]

After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs. Contrary to Wernicke's explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri. [8]

Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. [8] In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. [28] During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex. Today, with new neuroimaging techniques, we have been able to expand our knowledge on agnosia greatly. [3]

Related Research Articles

<span class="mw-page-title-main">Aphasia</span> Inability to comprehend or formulate language

In aphasia, a person may be unable to comprehend or unable to formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, epilepsy, autoimmune neurological diseases, brain infections, or neurodegenerative diseases.

<span class="mw-page-title-main">Receptive aphasia</span> Language disorder involving inability to understand language

Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, fluent 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 do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernicke's aphasia often suffer of anosognosia – they are 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.

<span class="mw-page-title-main">Head injury</span> Serious trauma to the cranium

A head injury is any injury that results in trauma to the skull or brain. The terms traumatic brain injury and head injury are often used interchangeably in the medical literature. Because head injuries cover such a broad scope of injuries, there are many causes—including accidents, falls, physical assault, or traffic accidents—that can cause head injuries.

Aphasiology is the study of language impairment usually resulting from brain damage, due to neurovascular accident—hemorrhage, stroke—or associated with a variety of neurodegenerative diseases, including different types of dementia. These specific language deficits, termed aphasias, may be defined as impairments of language production or comprehension that cannot be attributed to trivial causes such as deafness or oral paralysis. A number of aphasias have been described, but two are best known: expressive aphasia and receptive aphasia.

<span class="mw-page-title-main">Brain injury</span> Destruction or degeneration of brain cells

Brain injury (BI) is the destruction or degeneration of brain cells. Brain injuries occur due to a wide range of internal and external factors. In general, brain damage refers to significant, undiscriminating trauma-induced damage.

<span class="mw-page-title-main">Anomic aphasia</span> Medical condition

Anomic aphasia is a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say. By contrast, anomia is a deficit of expressive language, and a symptom of all forms of aphasia, but patients whose primary deficit is word retrieval are diagnosed with anomic aphasia. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used, but cannot find the appropriate word to name the object. Patients with anomic aphasia have relatively preserved speech fluency, repetition, comprehension, and grammatical speech.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

<span class="mw-page-title-main">Prosopagnosia</span> Cognitive disorder of face perception

Prosopagnosia, also known as 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 and intellectual functioning remain intact. The term originally referred to a condition following acute brain damage, but a congenital or developmental form of the disorder also exists, with a prevalence of 2.5%. The 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 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 specific for the recognition of human faces or if it is also involved in highly trained visual stimuli. Prosopagnosic patients are under normal conditions able to recognize facial expressions and emotions.

<span class="mw-page-title-main">Wernicke's area</span> Speech comprehension region in the dominant hemisphere of the hominid brain

Wernicke's area, also called Wernicke's speech area, is one of the two parts of the cerebral cortex that are linked to speech, the other being Broca's area. It is involved in the comprehension of written and spoken language, in contrast to Broca's area, which is primarily involved in the production of language. It is traditionally thought to reside in Brodmann area 22, which is located in the superior temporal gyrus in the dominant cerebral hemisphere, which is the left hemisphere in about 95% of right-handed individuals and 70% of left-handed individuals.

<span class="mw-page-title-main">Conduction aphasia</span> Medical condition

Conduction aphasia, also called associative aphasia, is an uncommon form of difficulty in speaking (aphasia). It is caused by damage to the parietal lobe of the brain. An acquired language disorder, it is characterised by intact auditory comprehension, coherent speech production, but poor speech repetition. Affected people are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as the person shows significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. People have frequent errors during spontaneous speech, such as substituting or transposing sounds. They are also aware of their errors and will show significant difficulty correcting them.

<span class="mw-page-title-main">Global aphasia</span> Medical condition

Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.

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").

<span class="mw-page-title-main">Language processing in the brain</span> How humans use words to communicate

In psycholinguistics, language processing refers to the way humans use words to communicate ideas and feelings, and how such communications are processed and understood. Language processing is considered to be a uniquely human ability that is not produced with the same grammatical understanding or systematicity in even human's closest primate relatives.

<span class="mw-page-title-main">Associative visual agnosia</span> Medical condition

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. Affected 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, language, memory, or 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.[2] There are two types of visual agnosia: apperceptive agnosia and associative agnosia.

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.

Focal neurologic signs also known as focal neurological deficits or focal CNS signs are impairments of nerve, spinal cord, or brain function that affects a specific region of the body, e.g. weakness in the left arm, the right leg, paresis, or plegia.

Apperceptive agnosia is a neurological disorder characterized by failures in recognition 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.

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 rather a neurological inability of the brain to process sound meaning. While auditory agnosia impairs the understanding of sounds, other abilities such as reading, writing, and speaking are not hindered. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway.

Phonagnosia is a type of agnosia, or loss of knowledge, that involves a disturbance in the recognition of familiar voices and the impairment of voice discrimination abilities in which the affected individual does not suffer from comprehension deficits. Phonagnosia is an auditory agnosia, an acquired auditory processing disorder resulting from brain damage. Other auditory agnosias include cortical deafness and auditory verbal agnosia also known as pure word deafness.

References

  1. "Agnosia". BrainFacts.org. Retrieved 15 August 2023.
  2. Kolb, Bryan; Whishaw, Ian Q. (3 March 2003). Fundamentals of Human Neuropsychology. Worth Publishers. ISBN   978-0-7167-5300-1.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 Burns, MS (2004). "Clinical management of agnosia". Top Stroke Rehabil. 11 (1): 1–9. doi:10.1310/N13K-YKYQ-3XX1-NFAV. PMID   14872395. S2CID   5758683. Archived from the original on 2013-01-28.
  4. 1 2 3 4 "NINDS Agnosia Information Page". National Institute of Neurological Disorders and Stroke. Archived from the original on 2013-01-27. Retrieved 2012-03-28.
  5. 1 2 "Agnosia". Archived from the original on 2017-05-26. Retrieved 2016-12-16.
  6. Zeki, S (1991). "Cerebral akinetopsia (visual motion blindness)". Brain. 114 (2): 811–824. doi:10.1093/brain/114.2.811. PMID   2043951.
  7. Riddoch MJ, Humphreys GW (May 2003). "Visual agnosia". Neurol Clin. 21 (2): 501–20. doi:10.1016/s0733-8619(02)00095-6. PMID   12916489.
  8. 1 2 3 4 Goldstein, Marvin N. (1974). "Auditory agnosia for speech ("pure word-deafness")". Brain and Language. 1 (2): 195–204. doi:10.1016/0093-934X(74)90034-0. ISSN   0093-934X.
  9. Vignolo, L. A (1982). "Auditory Agnosia". Biological Sciences. 298 (1089): 49–57. Bibcode:1982RSPTB.298...49V. doi:10.1098/rstb.1982.0071. PMID   6125975.
  10. Cowey A, Alexander I, Heywood C, Kentridge R (August 2008). "Pupillary responses to coloured and contourless displays in total cerebral achromatopsia". Brain. 131 (Pt 8): 2153–60. doi: 10.1093/brain/awn110 . PMID   18550620.
  11. Woodward, T. S; M. J Dixon; K. T Mullen; K. M Christensen; D. N. Bub (1999). "Analysis of errors in color agnosia: A single case study". Neurocase. 5 (2): 95–108. doi:10.1093/neucas/5.2.95.
  12. Zeki S (1990). "A century of cerebral achromatopsia". Brain. 113 (Pt 6): 1721–77. doi:10.1093/brain/113.6.1721. PMID   2276043.
  13. Van Lancker DR, Cummings JL, Kreiman J, Dobkin BH (June 1988). "Phonagnosia: a dissociation between familiar and unfamiliar voices". Cortex. 24 (2): 195–209. doi: 10.1016/s0010-9452(88)80029-7 . PMID   3416603. S2CID   28617313.
  14. Cherney LR (2004). "Aphasia, alexia, and oral reading". Top Stroke Rehabil. 11 (1): 22–36. doi:10.1310/VUPX-WDX7-J1EU-00TB. PMID   14872397. S2CID   218644618.
  15. Sakurai, Y (2004). "Varieties of alexia from fusiform, posterior inferior temporal and posterior occipital gyrus". Behavioural Neurology. 15 (1–2): 35–50. doi: 10.1155/2004/305194 . PMC   5488613 . PMID   15201492.
  16. Magnié MN, Ferreira CT, Giusiano B, Poncet M (January 1999). "Category specificity in object agnosia: preservation of sensorimotor experiences related to objects". Neuropsychologia. 37 (1): 67–74. doi:10.1016/S0028-3932(98)00045-1. PMID   9920472. S2CID   1550842.
  17. Coslett HB, Saffran E (August 1991). "Simultanagnosia. To see but not two see". Brain. 114 (4): 1523–45. doi:10.1093/brain/114.4.1523. PMID   1884165.
  18. Rizzo M, Vecera SP (February 2002). "Psychoanatomical substrates of Bálint's syndrome". J. Neurol. Neurosurg. Psychiatry. 72 (2): 162–78. doi:10.1136/jnnp.72.2.162. PMC   1737727 . PMID   11796765.
  19. Reed CL, Caselli RJ, Farah MJ (June 1996). "Tactile agnosia. Underlying impairment and implications for normal tactile object recognition". Brain. 119 (3): 875–88. doi:10.1093/brain/119.3.875. PMID   8673499.
  20. Mendez, Mario F; Cherrier, Monique M (2003). "Agnosia for scenes in topographagnosia". Neuropsychologia. 41 (10): 1387–1395. doi:10.1016/S0028-3932(03)00041-1. PMID   12757910. S2CID   9021982.
  21. Greene JD (December 2005). "Apraxia, agnosias, and higher visual function abnormalities". J. Neurol. Neurosurg. Psychiatry. 76 (Suppl 5): v25–34. doi:10.1136/jnnp.2005.081885. PMC   1765708 . PMID   16291919.
  22. 1 2 3 4 Galotti], Kathleen M. (2010). Cognitive psychology : in and out of the laboratory (1st Canadian ed.). Canada: Nelson. ISBN   978-0-17-644065-7.
  23. Silverman, Gordon; Friedenberg, Jay (2011-07-14). Cognitive science : an introduction to the study of mind (2nd ed.). Thousand Oaks, Calif.: SAGE. ISBN   978-1-4129-7761-6.
  24. 1 2 3 4 Howard, Harry. "The superior temporal sulcus". Brain and Language. Archived from the original on 22 December 2015. Retrieved 6 December 2015.
  25. "The New Yorker: From the Archives: Content". The New Yorker . Archived from the original on 2006-08-31. Retrieved 2010-05-05. mentally blind, or agnosic—able to see but not to decipher what he was seeing.
  26. "ClinicalTrials.gov".
  27. "Freud 1891">Freud, Sigmund, Zur Auffassung der Aphasien, Vienna, 1891, p. 80
  28. Vecera, P. S; Gilds, S. K (1998). "What processing is impaired in appreceptive agnosia? Evidence from normal subjects". Journal of Cognitive Neuroscience. 10 (5): 568–580. doi:10.1162/089892998562979. PMID   9802990. S2CID   21568462.