Flashcards in Agnosia Deck (20):
- Damage to the earliest visual brain areas cause ______. (1)
- Damage to brain areas further along the visual information processing pathway cause an inability to process _______(2)
- Damage even further along causes _______(3), but intact processing of basic features.
1. Blindness (scotomas)
2. Features of a stimulus (e.g., colour [achromatopsia V4], motion [akinetopsia MT] etc.
3. Object recognition deficits (visual agnosia; LOC, FFA etc.)
Given that information in visual images is processed in a hierarchical fashion....
Processing of elementary visual features (lines, angles, edges, colour, curves, motion) is processed ______(1).
More complex aspects of visual information (e.g., object form, spatial representations are processed _____ (2), via the ____(3) ("what") and _____ (4) ("where") brain pathways.
1. Early! (E.g., orientation-selective special cells in the occipital cortex).
3. Ventral (deficits in object recognition)
4. Dorsal (deficits in spatial)
Ventral and dorsal split off from the
Damage to the "what" (Ventral) pathway can result in what types of perceptual deficit?
Ventral simultanagnosia (meaning of multiple objects)
Damage to the 'where' pathway can result in what types of perceptual deficits?
Dorsal simultanagnosia (spatial processing of multiple objects)
What is he difference between apperceptive and associative agnosia?
They affect different 'stages' of visual processing.
Sensation is intact in both conditions. However, In apperceptive agnosia the deficit occurs earlier is processing (occipital vision areas) and patients have difficulty forming visual representations of visual images/shapes/objects (and therefore have difficulty recognising and copying images). In contrast in associative agnosia reflects "recognition without meaning" due to damage later in the ventral system - these patients may be able to copy a visual image, but not be able to recognise what it is! (but could if it were described to them).
Therefore, a distinction can be made via tests of 'copying' versus drawing from mind.
Apperceptive agnosias (also known as visual space agnosias) refer to a condition in which a person fails to recognize objects due to a functional impairment of the occipito-temporal vision areas of the brain. Other elementary visual functions such as acuity, colour vision, and brightness discrimination are still intact. Apperceptive agnosics are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli.
Associative agnosias are also known as visual object agnosias. Although they can present with a variety of symptoms, the main impairment is a failure to recognize visually presented objects despite having intact perception of that object. A patient with an associative agnosia may be able to replicate a drawing of the object but still fail to recognize it. Errors in misidentifying an object as one that looks similar are common. Three specific criteria are associated with a diagnosis of associative agnosia (Farah,1990):
1) Difficulty recognizing a variety of visually presented objects (e.g., naming or grouping objects together according to their semantic categories).
2) Normal recognition of objects from a verbal description of it or when using a sense other than vision such as touch, smell, or taste.
3) Elementary visual perception intact sufficient to copy an object, as exemplified in original and copied picture below.
Overall, this loss can be thought of as "recognition without meaning".
Describe the three-stage model of object perception.
(optional - draw it)
Visual image --> process local features (edges and lines) --> process shape representation (shapes and surfaces) --> object recognition (its a cows face!)
What is apperceptive agnosia?
What type of neuroanatomical damage is linked with this kind of agnosia?
Impaired shape identification, impaired copying/matching/tracing, difficulty judging line orientation (horizontal vs/ vertical) - affects ALL kinds of visual stimuli (words/objects/faces)
- can reach for objects accurately and negotiate a path
- acuity, brightness discrimination, and colour vision (visual senses) are all ok!
Apperceptive agnosia the deficit occurs earlier is processing (occipital [sometimes parietal] vision areas) and patients have difficulty forming visual representations of visual images/shapes/objects (and therefore have difficulty recognising and copying images). Theories to be due to a deficit in perceptual group processes such as that outlined by the gestalt psychologist (e.g., proximity, similarity, closure, good continuation etc).
Typically occurs after gross bilateral damage to occipital (sometimes parietal lobes), particularly where damage is diffuse (Rather than focal) e.g., carbon monoxide poisoning.
What is the peppery-mask theory of apperceptive agnosia?
That multiple sites of damage to the visual cortex leads to multiple, various sized, blind spots. producing apperceptive agnosia.
What is the 'grouping hypothesis' of apperceptive agnosia?
That apperceptive agnosia is a deficit in perceptual grouping processes such as that outlined by the gestalt psychologist (e.g., proximity, similarity, closure, good continuation etc).
For apperceptive agnosia, is there more support for the peppery mask or the grouping hypothesis?
Grouping hypothesis - That apperceptive agnosia is a deficit in perceptual grouping processes such as that outlined by the gestalt psychologist (e.g., proximity, similarity, closure, good continuation etc).
What is prosopagnosia?
What type of neuroanatomical damage is it associated with?
- a VISUAL impairment in recognising familiar faces (#person recognition can occur non-visually and memory is intact)
Bilateral mid-fusiform lesions
What does it mean to say that associative agnosias can be 'material specific'? (give examples)
The agnosia may only occur for a specific subtype of materials
Letters -> pure alexia
Faces -> prosopagnosis
Unable to navigate using cues/landmarks -> topographical agnosia
How is associative agnosia differentiated from optic aphasia?
In short, agnosia is a recognition problem, optic aphasia is a naming problem.
In optic aphasia (Associated with callosal disconnection/ a patient cannot name objects presented visually - BUT they can demonstrate use by gesturing - agnostics CANNOT, because they are unable to draw a link between the visual form and semantics.
What is associative agnosia?
What type of neuroanatomical damage is linked with this kind of agnosia?
- Impaired recognition of complex forms and objects (what is this a picture of!), early visual processing is much more intact (can copy and match! and some can draw from memory). Can access semantics - BUT NOT VIA VISUAL IMAGERY!
Classically considered perception stripped of meaning , however, some stored knowledge can be intact (some can draw from memory) and context can be helpful (i.e., better with real objects in scenes than isolated drawings).
Lesions typically bilateral ventral (occipital-temporal pathway)
In prosopagnosia, what aspects of facial processing may be spared?
- Recognition that a face is a face (just not which one!)
- age and gender
- facial emotion
What is the 'expertise' theory of facial processing?
The notion that the processing of faces merely appears to be different from objects because we are experts with faces, but not most objects - and that the same system can be invoked for other domains of expertise when we become very good at recognising visually similar objects (supported by neuroanatomical and behavioural studies of car expert/ bird expert)
that the system responsible for face processing is also recruited for the identification of non-face objects of expertise!
there is not necessarily a special brain region or process specific to the processing of faces -- but rather that the appearance of 'specific' deficits in facial processing occurs because humans are 'experts' in face processing ---- but that the same process and brain regions are in fact used to process visual material that is the center of other areas of expertise (Dog experts, care experts etc).
[THINK ABOUT GREBLE STUDY - people trained to become greeble experts ... gradually show more activation in fusiform face area as their expertise grows! ]
We tend to process faces _____, but this is less likely to occur when a face is _____
1. Holistically (E.g., two face halves, top and bottom, put together
What did patient CK/SM suggest about the processing of faces/face recognition?
(CK could recognise faces but not objects e.g., could see a face made up of vegetables, but not recognise the vegetables it was made up ok; but he suffered more when faces were inverted than controls did)
SM can recognise objects, but not faces
Both poor at discriminating similar objects.
That face recognition normally depends on two systems
1. a holistic/expert system that is dependent on orientation-specific coding of second-order relational features (internal) [intact in CK, damaged in SM] [later part of the model]
2. a part-based object recognition system which contributes to face recognition when stimulus does not satisfy the domain-specific conditions needed to activate the expertise/face system [damaged in CK, intact in SM] [earlier part of model]
What happened when they trained SM to become a greble expert?
What does this suggest about face vs non-face processing?
(SM can recognise objects, but not faces)
gained ability to discriminate between greebles...but began to lose even more of his ability to discriminate between faces!!
- suggests the potential for experience-dependent dynamic reorganisation in agnosia. Suggests that face and non-face processing may compete for resources.