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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: appreceptive agnosia and associative agnosia.[1] Individuals with appreceptive agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Appreceptive agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere. [1] In contrast, individuals with associative 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. [1]. A specific form of associative agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers [1]. However, individuals with prosopagnosia can recognize all other types of visual stimuli[2].

Changes to be made to page:

I will be making changes to the agnosia page in the upcoming weeks. I am doing this for a university assignment under the Association for Psychological Sciences initiative. The following are changes that I am planning to make based on reading previous comments on the talk page for the agnosia page:

I plan to provide a reference for automobilia agnosia, as it was noted that there is no reference for it. I plan on alphabetizing the list of all of the types of agnosia. I plan on creating a citation tag for prosopagnosia. I would also like to add topographical agnosia to the list.

Ideas of my own to improve the page are to add a section about patient DF who had a form of visual agnosia. Patient DF suffered from damage to lateral parts of the occipital lobe. She was unable to make copies of drawings or objects given to her, nor was she able to recognize the drawings or objects (Milner & Goodale, 1995). Interestingly, patient DF was able to successfully complete part of a card slot task (Allard, 2001) which I will expand upon in the section I add about patient DF.

Another section I would like to add to the agnosia page, is a section on Lissauer. Lissauer was one of the first theorists about agnosia (Vecera, 1998). This will provide a bit of background behind different theories about agnosia. Additionally I would like to add more information on the dorsal and ventral streams, as these play large roles in agnosia.

Lastly, I would like to add to the treatment and causes sections, as I believe they are sparse right now and adding information to them will increase the usefulness of the page on agnosia.

I may also add pictures showing different regions of the brain that are affected for certain forms of agnosia, specifically for appreceptive and associative agnosia. As well as diagrams showing both the dorsal and ventral streams

Reference work:

The following are some of the subheadings which I would like to add, and areas that I would like to add on to.

Agnosia

Agnosia only occurs in a single modality for example vision or hearing may be affected [3].

Patient DF

Patient DF suffered from bilateral damage to the ventral stream [4]. However DF's dorsal stream remained intact. This damage to the ventral stream caused Patient DF to develop visual form agnosia. DF struggled with visual recognition and was unable to recognize simple shapes, or distinguish between them. Additionally, DF could not tell the orientation or width of an object. However, DF was able to make copies of the orientation of a line when given an unlimited amount of time. In another task DF was presented with a square and an oblong object. DF was then asked to indicate which of the objects was a square and which of the objects was oblong. When DF was able to pick up the objects she was able to determine which of the objects was a square and which was oblong, but when she was required to answer only verbally she could not correctly determine the shape [5].

Dr. P

Oliver Sacks, a neurologist tells the story of his fascinating patient Dr. P. Dr. P was an average man who taught music at the university level and who is now commonly known as the man who mistook his wife for a hat. He had issues recognizing students as they approached him, but once they spoke he could identify who the student was. Dr. P was unable to see whole pictures and could only focus on the features of the picture or small pieces of it. For example in a picture depicting a lake, mountains and forests, he would only be able to focus on the mountains. After one appointment with Dr. Sacks, Dr. P got up and tried to lift his wife's head because he thought that her head was his hat. Dr. P suffered from a form of visual agnosia, specifically prosopagnosia. He also suffered from a form of neglect syndrome. When asked to visualize himself walking down a hallway, he would only describe the right side of the hallway and neglect the left side [6]. Lissauer

Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul [7] . 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 damage, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object [8]. 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 [9].

Wernicke

Some of the first ideas about agnosia came from Wernicke who created theories about sensory aphasia in 1874. He noted that individuals with sensory aphasia did not possess the ability to understand speech or repeat words. He believed that sensory aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with sensory aphasia had a limited deafness for certain sounds and frequencies in speech [10].

Kussmaul

After Wernicke, came Kussmaul in 1877 who attempted to explain why word deafness occurs. Contrary to Wernicke's explanations, Kussmaul believed word deafness as the result of major destruction of the first left temporal gyrus. Kussmaul also posited about the origins of word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri [11].

Topographagnosia

This form of agnosia involves the inability to recognize landmarks. Patients with topographagnosia have the ability to read maps, but become lost in familiar environments [12].

Dorsal Simultanagnosia

Simultanagnosia broadly refers to the inability recognize more than one object at once. For example a patient for dorsal simultanagnosia may report seeing only one of four objects that are lined up in front of them. Individuals with dorsal simultanagnosia often use parts of an object to make inferences about an object as a whole. These individuals also have difficulty with reading and counting because it involves more than one object at a time. Dorsal simultanagnosia is commonly caused by bilateral damage to the bilateral parieto-occipito region [13].

Ventral Simultanagnosia

Individuals with ventral simultanagnosia are unable to identify more than one object at a time. However, they can see more than one object at a time. These individuals also experience difficulty reading and describing pictures with multiple features. Ventral simultanagnosia is commonly caused by damage to the left inferior tempero-occipital regions of the brain [14].

Color Agnosia

Color agnosia involves having difficulty categorizing colours, as well as recognizing colours. Colour agnosia is usually caused by neurological damage [15]. 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 will result known as hemiachromatopsia [16].

Environmental Agnosia It 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 [17].

Integrative agnosia Usually a patient has a form of associative agnosia or appreceptive agnosia. However, in the case of integrative agnosia a patient falls in between a form of associative and appreceptive agnosia [18].


Assessing Agnosia

In order to assess an individual for agnosia, it must be verified that the individual is not suffering from 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 appreceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual is suffering from a form of appreceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual is suffering from a form of associative agnosia, they will not be able to match different examples of stimuli. 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 [19].

Testing for 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 helps in identifying the face such as "Who sang the song Borderline?" [20].

Testing for Alexia Patients with alexia often have damage to their corpus collosum, as well as damage to the left visual association areas [21]. 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. However, individuals with pure alexia show a frequency effect. They are able read high frequency words better and faster than they can read low frequency words [22].

Testing for Congenital Amusia A tested known as the Montreal Battery for the Evaluation of Amusia (MBEA) can be administered to an individual to test for congenital amusia. The MBEA consists of seven subtests that test for music perception and memory, time dimension and incidental memory [23].

Testing for Alexia Individuals with alexia usually have difficulty reading words as well as with identifying letters. In order to assess whether an individual has alexia, tests of copying and recognition must be performed. An individual with alexia should be able to copy a set of words, and should be able to recognize letters [24].

Alexithymia

An individual suffering from alexithymia experiences difficulty in emotional self regulation and alexithymia is a possible risk factor for certain psychiatric disorders. There are five major defining factors of alexithymia: a reduced ability or incapability to experience emotions, verbalize emotions or fantasize. Additional characteristics of alexithymia involve an absence in reflection and thought about one's emotions and difficulty in identifying emotions. Alexithymia can be divided into two different types: axis I alexithymia and axis II alexithymia. Axis I alexithymia involves the inability to experience emotion, as well as the absence of the cognitive aspects that accompany emotions. Axis II alexithymia is a selective deficit. Only the cognitive aspects associated with emotions are affected, while the ability to have emotional experiences remains intact [25].

Auditory Agnosia

Auditory agnosia has been recognized since 1877 [26]. Auditory agnosia involves a deficit in recognizing non-verbal sounds or noises. There are two types of auditory agnosia: semantic associative and discriminative agnosia. Semantic associative agnosia is associated with lesions to the left hemisphere, where as discriminative agnosia is associated with lesions to the right hemisphere [27].

Cerebral Akinetopsia

Cerebral akinetopsia is associated with the inability to perceive visual motion. One cause of cerebral akinetopsia is lesions outside the striate cortex [28].

Alexithymia

Alexithymia involves an impairment in emotional regulation [29].

Congenital Amusia

Congenital amusia refers to a deficit in musical processing. One of the deficits involved in congenital amusia is the inability to recognize familiar songs. Congenital amusia occurs without brain damage [30]. Congenital amusia affects about 4% of the population [31].

Mirror Agnosia

Commonly due to a right parietal lesion [32].

Causes

Agnosia may be caused by stroke, dementia, developmental disorders or other neurological conditions. 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 [33].

Treatment

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This is known as 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 it's 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 [34].

Compensatory strategies with alternate modalities: These strategies elicit the use of an unaffected modality. For example visual agnosics can use tactile information in replacement of visual information. Alternatively, an individual with prosopagnosia can use auditory information in order to replace visual information. They can wait for someone to speak, and will usually recognize the individual from their speech.

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 off of this description more easily than through visual cues.

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 cues such as a scar on an individual's face or crooked teeth in order to recognize the individual.

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.

Pictures File:Ventral-dorsal streams.svg File:Fusiform gyrus animation.gif

Picture of the ventral and dorsal streams
Animation of the fusiform area, the area damaged in prosopagnosia.


References

[edit]

[35] [36] [37] [38] [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] [51] [52] [53] [54] [55] [56]

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  3. ^ "NINDS Agnosia Information Page". National Institute of Neurological Disorders and Stroke. Retrieved 28 March 2012.
  4. ^ Schenk, T (2006). "An allocentric rather than perceptual deficit in patient D.F". Nature Neuroscience. 11 (9): 1369–1370. doi:10.1038/nn1784. PMID 17028584.
  5. ^ Milner, D (1998). "Streams and consciousness: visual awareness and the brain". Trends in Cognitive Sciences. 2 (1): 25–30. doi:10.1016/S1364-6613(97)01116-9. PMID 21244959.
  6. ^ Pinel, John P.J. (2011). Biopsychology (8th ed.). Boston: Allyn & Bacon. ISBN 978-0205832569.
  7. ^ Goldstein, M. N (1974). "Auditory agnosia for speech". Brain and Language. 1: 195–204. doi:10.1016/0093-934X(74)90034-0.
  8. ^ Vecera, P. S (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  9. ^ Burns, M (2004). "Clinical Management of Agnosia". Top Stroke Rehabilitation. 11 (1): 1–9. doi:10.1310/N13K-YKYQ-3XX1-NFAV. PMID 14872395.
  10. ^ Goldstein, M. N (1974). "Auditory agnosia for speech". Brain and Language. 1: 195–204. doi:10.1016/0093-934X(74)90034-0.
  11. ^ Goldstein, M. N (1974). "Auditory agnosia for speech". Brain and Language. 1: 195–204. doi:10.1016/0093-934X(74)90034-0.
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  20. ^ Burns, M (2004). "Clinical Management of Agnosia". Top Stroke Rehabilitation. 11 (1): 1–9. doi:10.1310/N13K-YKYQ-3XX1-NFAV. PMID 14872395.
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  34. ^ Burns, M (2004). "Clinical Management of Agnosia". Top Stroke Rehabilitation. 11 (1): 1–9. doi:10.1310/N13K-YKYQ-3XX1-NFAV. PMID 14872395.
  35. ^ Silverman, Jay Friedenberg, Gordon (14 July 2011). Cognitive science : an introduction to the study of mind (2nd ed.). Thousand Oaks, Calif.: SAGE. ISBN 9781412977616.{{cite book}}: CS1 maint: multiple names: authors list (link)
  36. ^ Pinel, John P.J. (2011). Biopsychology (8th ed.). Boston: Allyn & Bacon. ISBN 978-0205832569.
  37. ^ "Types of Agnosias". University of Calgary. Retrieved 28 March 2012.
  38. ^ "Dorsal Simultanagnosia". University of Calgary. Retrieved 28 March 2012.
  39. ^ "Ventral Simultanagnosia". University of Calgary. Retrieved 28 March 2012.
  40. ^ "NINDS Agnosia Information Page". National Institute of Neurological Disorders and Stroke. Retrieved 28 March 2012.
  41. ^ Goldstein, M. N (1974). "Auditory agnosia for speech". Brain and Language. 1: 195–204. doi:10.1016/0093-934X(74)90034-0.
  42. ^ Ramachandran, V. S (1997). "Mirror Agnosia". Biological Sciences. 264 (1382): 645–647. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  43. ^ Milner, D (1998). "Streams and consciousness: visual awareness and the brain". Trends in Cognitive Sciences. 2 (1): 25–30. doi:10.1016/S1364-6613(97)01116-9. PMID 21244959.
  44. ^ Larsen, J (NaN undefined NaN). "Cognitive and emotional characteristics of alexithymia A review of neurobiological studies". Journal of Psychosomatic Research. 54 (6): 533–541. doi:10.1016/S0022-3999(02)00466-X. PMID 12781307. {{cite journal}}: Check date values in: |date= (help)
  45. ^ Tillmann, Barbara; Schulze, Katrin; Foxton, Jessica M. (NaN undefined NaN). "Congenital amusia: A short-term memory deficit for non-verbal, but not verbal sounds". Brain and Cognition. 71 (3): 259–264. doi:10.1016/j.bandc.2009.08.003. PMID 19762140. {{cite journal}}: Check date values in: |date= (help)
  46. ^ Vecera, P. S (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
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  49. ^ Zeki, S (1991). "Cerebral akinetopsia (visual motion blindness)". Brain. 114 (2): 811–824. doi:10.1093/brain/114.2.811. PMID 2043951.
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  53. ^ Vignolo, L. A (1982). "Auditory Agnosia". Biological Sciences. 298: 49–57.
  54. ^ Michel, F (2004). "Seeing without the occipito-parietal cortex: simultagnosia as a shrinkage of the attentional visual field". Behavioural Neurology. 15 (1–2): 3–13. doi:10.1155/2004/836830. PMC 5488620. PMID 15201489. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  55. ^ Platz, T (1996). "Tactile agnosia: Casuistic evidence and theoretical remarks on modality specific meaning representations and sensorimotor integration". Brain. 119: 1565–1574. doi:10.1093/brain/119.5.1565. PMID 8931580.
  56. ^ Binkofski, F (1999). "Mirror agnosia and mirror ataxia constitute different parietal lobe disorders". Annals of Neurology. 46 (1): 51–61. doi:10.1002/1531-8249(199907)46:1<51::AID-ANA9>3.0.CO;2-Q. PMID 10401780. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
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