Neuropsychology: The Seeing Brain Flashcards

1
Q

What kind of process is seeing?

A

-Complex (hierarchical) process
-Constructive process
-Example: Kanisza illusion

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2
Q

How is seeing a complex process?

A

-Eyes and brain play important roles
-Psychological and cognitive models: how does visual perception happen and which processes are involved

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3
Q

How is seeing a constructive process?

A

Things are added to input and interpreted in certain way

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4
Q

What is the Kanizsa illusion?

A

-Hard to perceive stimulus as three corners rather than triangle
-Triangle seen because stimulus gives impression of lines forming triangle
-Visual system in brain involved

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5
Q

What is the hierarchical system of seeing?

A

-Start in retina
-Lateral geniculate nucleus (LGN) in thalamus
-Secondary visual cortex
-Third region
-Fourth region
-Fifth region (MT) and other regions at same time
-Parietal regions, inferior temporal regions and frontal regions (FEF, frontal eye field)
-Lastly hippocampus
(image)

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6
Q

What are characteristics of the retina?

A

-First step in seeing
-Internal surface of eyes consisting of multiple layers
-Contains specialized photoreceptors to covert light into neural signals: rod cells and cone cells
-Optic nerves relay output of retinal ganglion cells to brain
-Blindspot: point at which optic nerve leaves eye, so no rods and cones present

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7
Q

What are rod cells?

A

-In retina of eye
-Specialized for low levels of light intensity
-More active during night time
-Evenly distributed across retina, but not present in fovea

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8
Q

What are cone cells?

A

-In retina of eye
-Specialized for detecting different wavelengths of light
-More active during day time
-Highest concentration in fovea

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9
Q

What is the geniculostriate pathway?

A

-Dominant pathway from retina to brain: travels to primary visual cortex (V1) at back of brain
-Certain part of visual fields might no longer be seen when damage somewhere in pathway
-Lateral geniculate nucleus (LGN): transfers visual information through neurons inside
-Primary visual cortex (V1, striate cortex): extracts basic info from visual scene

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10
Q

Which route does the geniculostriate pathway follow?

A

-Each retina has part for right stimuli and left stimuli
-Optic nerves receive info and half of them cross in optic chiasm
-Other parts of optic nerve stay on same side of brain and come together with opposite optic nerve in optic tract, so both hemispheres get input from both eyes
-In lateral geniculate nucleus (LGN), input from left and right eye stays separate in different layers
-Primary visual cortex combines input from both eyes and passes it on to further regions

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11
Q

What kinds of conditions can be the result of damage somewhere in the geniculostriate pathway?

A

-Monocular blindness: damage to eye or optic nerve
-Bitemporal hemianopia: damage in crossing fibers of optic chiasm
-Right nasal hemianopia: damage in nerve that doesn’t cross
-Homonymous hemianopia: abscence of optic tract or lateral geniculate nucleus (LGN)
-Quadrantanopia: damage in part of optic tract or lateral geniculate nucleus (LGN)
-Macular sparing: damage in primary visual cortex

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12
Q

What are characteristics of the lateral geniculate nucleus (LGN)?

A

-Transfers visual information through neurons inside
-6 layers: 3 for each eye
-Cells have center-surround receptive field
–>Respond to contrast: differences in light between center and surround of receptive field
–>Don’t like overall light or overall dark

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13
Q

What are characteristics of the primary visual cortex (V1, striate cortex)?

A

-Extracts basic info from visual scene
-Info used by later stages of processing to extract info about shape, color, movement, etc.
-Hubel & Wiesel: single-cell recordings showed there’s hierarchy in processing in primary visual cortex
-Spatial arrangement of primary visual cortex: representation of whole visual field of one side combined in primary visual cortex
–>Retinotopic organisation
–>Damage to parts in primary visual cortex results in blindness for corresponding region of space

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14
Q

What are the stages of cells in the primary visual cortex according to Hubel & Wiesel?

A

-Simple cells: derive response by combining responses of several LGN center-surround, respond to different orientations
-Complex cells: derived by combining responses of several simple cells, respond to orientation but have larger receptive field and require stimulation on entire length
-Hypercomplex cells: outside V1, derived by combining responses of several complex cells, sensitive to length AND orientation

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15
Q

Which types of cells can be found in the primary visual cortex (V1)?

A

-Simple cells: derive response by combining responses of several LGN center-surround cells, respond to different orientations
-Complex cells: derived by combining responses of several simple cells, respond to orientation but have larger receptive fields and require stimulation on entire length
-Hypercomplex cells (outside V1): derived by combining responses of several complex cells, sensitive to length AND orientation

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16
Q

What is retinotopic organisation?

A

-Different neurons will see different parts of visual field
-Spatial arrangement of light on retina retained in response properties of primary visual cortex-neurons, but inverted (top part of primary visual cortex is bottom of visual space and vice versa)

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17
Q

What kind of blindness can be the result of damage to parts of the primary visual cortex?

A

-Hemianopia: fully damaged primary visual cortex in one hemisphere
-Scotoma: small damaged primary visual cortex in one hemisphere
-Quadrantanopia: half damaged primary visual cortex in one hemisphere

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18
Q

Why is the place of damage important?

A

-Still residual vision if damage happens further in pathway, like primary visual cortex
-Reason: multiple pathways from eye to brain
–>Geniculostriate pathway most well understood and makes largest contribution to human visual perception
–>Other routes evolutionary more ancient

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19
Q

What are the consequences of the geniculostriate pathway being the most important for conscious vision?

A

-Damage to pathway impairs conscious vision
-But other aspects spared
-Example: blindsight

20
Q

What is blindsight?

A

-Damage to V1: patient cannot consciously report objects presented in this region of space
-But patient still able to make visual discriminations in blind area (orientation, movement direction)

21
Q

What are characteristics of blindsight?

A

-Possible because of other routes from eye to brain: routes for unconscious vision
-More blindsight if damage is in both hemispheres
-Filling-in of blind regions: regions filled up with something expected to be there
-Low trust in tasks because can’t consciously see, but does task well
-Remaining vision not great, so small obstacles will probably make patient trip
-Example of how visual perception is constructed

22
Q

What other regions are involved in seeing?

A

-Prestriate regions: V2, V3, V3a, V4, V5/MT
-Non-visual cortical areas: temporal and parietal cortex
–>Ventral what stream: to temporal lobe
–>Dorsal where stream: to parietal lobe

23
Q

What is the V4 area?

A

-Main color center of brain
-Brain needs specialized processing system for color, although retina is already sensitive to different wavelengths of light
-Area V4 computes color of object taking into account variations in lighting conditions (color constancy)
-Damage in V4: achromatopsia

24
Q

Why does the brain need a specialized processing system for color, while the retina is already sensitive to different wavelengths of light?

A

-Problem: wavelength depends on composition of light source and color of object
–>Retina not specialized enough to compare wavelengths and discount effect of illumination
-Color constancy: V4 computes color of object taking into account variations in lighting conditions
–>Cells in V4 continue to respond to same surface color if light source is changed
–>Cells is V1 don’t respond to same surface color if light source is changed

25
Q

What is achromatopsia?

A

-Patients with damage in V4
-Fail to see all color: seeing world in black and white
-Retina and cells in primary visual cortex still respond to different wavelengths of light
-Not same as color blindness (due to cone deficiency)
-Example of how visual perception is constructed

26
Q

What is the V5/MT area?

A

-Main movement center of brain
-90% of cells in V5/MT respond to particular direction of movement (direction sensitivity)
-Bilateral damage in V5/MT: akinetopsia
-More regions involved in movement, especially in complex movements (biological motion)
–>Involvement of posterior superior temporal sulcus

27
Q

What is biological motion?

A

-Possible to discriminate biological from random motion, given array of moving dots
-Brain imaging and neuropsychology suggest that this may use additional regions/mechanisms beyond ones involved in determining overall direction of movement (system), including posterior superior temporal sulcus
-Akinetopsic patients can discriminate biological motion

28
Q

What is akinetopsia?

A

-Bilateral damage in V5/MT
-Fail to see movement: seeing world in series of still frames, not how frames change
-Possible to detect movement with other senses
-Quite rare

29
Q

What is needed beyond the visual cortex to see?

A

-Visual cortex (striate and extrastriate) extracts basic info (colors, movement, shapes, edges)
-In order to be able to use info, needs to make contact with other types of info
–>Where object is in space (can’t be computed from retinal image alone)
–>What object is
-Leads to model of object recognition

30
Q

How is all the visual info put together to form a coherent perception according to the model of object recognition?

A

-1st: early visual processing (color, motion, edges, etc.) (already seen in previous part)
-2nd: grouping of visual elements (gestalt principles, figure - ground segmentation)
-3rd: matching grouped visual description to representation of object stored in brain (structural descriptions)
-Attaching meaning to object (retrieved from semantic memory)
(image)

31
Q

What consequences can damage in different stages of model of object recognition have?

A

-Damage in mid- or higher visual processes: visual agnosia
-Damage in grouping visual elements: integrative and visual form agnosia
-Damage in matching visual description to structural descriptions: object orientation agnosia
-Apperceptive agnosia
-Associative agnosia

32
Q

What is visual agnosia?

A

-Due to damage in mid- and/or higher-order visual processes
-Problem in: mid- and/or high-order visual processes necessary to recognize objects based on vision
-Intact: low-level visual processes (motion, color, etc.)
-Intact knowledge about objects and thus intact recognition based upon other modalities (hearing voice, etc.) and intact alertness, intelligence, language
-2 types: apperceptive agnosia and associative agnosia
–>Clinically useful, but too simplistic (many stages in system)

33
Q

What is apperceptive agnosia?

A

-Type of visual agnosia
-Disorder in forming coherent visual representation
-2 types: integrative and visual form agnosia

34
Q

What is associative agnosia?

A

-Type of visual agnosia
-Disorder in recognition and linking despite intact visual representation

35
Q

Which Gestalt principles are there to combine parts into a whole?

A

-Law of proximity
-Law of similarity
-Law of good continuation
-Law of closure

36
Q

What is integrative agnosia?

A

-Damage in grouping visual elements (constitutes to 2nd stage of model of object recognition)
-Type of apperceptive agnosia in which grouping principles are disrupted
-Inability to form whole of visual image
-Slightly different symptoms per patient possible
-Spared: copying pictures, drawing from memory
-Impaired: deciding if objects are real or not, naming objects, naming objects that overlap each other

37
Q

What is visual form agnosia?

A

-Damage in grouping visual elements
–>Could be because of bilateral damage to lateral occipital cortex
-Type of apperceptive agnosia (but borderline)
-Inability to form representation
-Impaired: unable to copy or recognize line drawings of objects
-Spared: can recognize real objects based on color/texture, intact memory of objects (drawing from memory), can interact with objects (ex.: doesn’t know what hammer is, but can use it)

38
Q

What is object constancy?

A

-Achieved by mapping potentially infinite number of visual depictions onto finite set of stored descriptions of object structure
-Suggestion: brain stores objects in single viewpoint (canonical viewpoint that contains principle axis)
–>Implication: object recognition involves view normalization from seen viewpoint to stored viewpoint (mental rotation)
-Another suggestion: stored structural description accessed by matching feature-by-feature
-Modern terminology: invariance/tolerance

39
Q

What are the neural substrates of object constancy?

A

-Monkey cells in inferotemporal cortex respond to very particular object attributes (corners, shapes), but less concerned with where located in space
–>Ideal conditions for computing object constancy
-fMRI in humans: inferotemporal regions respond to same object presented in different sizes: left region insensitive to viewpoint, right region sensitive to viewpoint
–>Consistent with 2 different routes to object constancy

40
Q

What is object orientation agnosia?

A

-Right parietal lobe damage
-Damage in matching visual description to structural descriptions
-Inability to normalize viewpoints
-Spared: able to recognize object in all viewpoints (unusual and canonical)
-Impaired: unable to choose correct orientation for object
-Provides evidence that principle axis is stored separately from other aspects of object recognition

41
Q

Which areas in the higher ventral vision pathway are associated with different object categories?

A

-Fusiform face area (FFA): for faces
-Extrastriate body area (EBA): for bodies
-Parahippocampal place area (PPA): for scenes
-Visual word form area (VWFA): for word forms

42
Q

What is special about faces?

A

-Face recognition: within-category discrimination (meaning all faces look same), whereas other object recognition is between category (ex: distinguishing pen from cup)
-Faces might use different types of processing
-Faces might be/have been important from social/evolutionary perspective: domain specificity
–>But might also be based upon experience
-Evidence that faces are special: prosopagnosia

43
Q

Which different aspects of face processing did Bruce & Young find (1986)?

A

-Important proposals
–>Distinction between processing familiar and unfamiliar faces (unfamiliar faces: direct route)
–>Specific route for expression
–>Specific route for facial speech
-Different kinds of evidence found
-Processing towars: face recognition units = structural descriptions (view-invariant)

44
Q

What kind of evidence is there for the Bruce & Young model of processing faces?

A

-Face constancy: double dissociation between recognizing familiar faces and matching unfamiliar faces across different viewing conditions
-Face naming: often possible to retrieve semantic facts without retrieving name, but reverse pattern not found (name generation depends on semantic retrieval)
-Double dissociation between recognizing familiar faces and recognizing emotion, age and sex
-Double dissociation between recognizing familiar faces and using lip-reading cues

45
Q

What brain regions were connected to different processes of face recognition by Haxby et al. (2000)?

A

fMRI
-Core system: for visual analysis
–>Inferior occipital gyri: early perception of facial features
–>Lateral fusiform gyrus (FFA): invariant aspects of faces - perception of unique identity
–>Superior temporal sulcus (STS): changeable aspects of faces - perception of eye gaze, expression, and lip movement
-Extended system: for further processing
–>Intraparietal sulcus: spatially directed attention
–>Auditory cortex: prelexical speech perception
–>Amygdala, insula, limbic system: emotion
–>Anterior temporal: personal identity, name and biographical information
(image)

46
Q

What is prosopagnosia?

A

-Impairment in general face processing that doesn’t reflect difficulties in early visual analysis
–>Used specifically to refer to difficulty in recognizing previously familiar faces
-Congenital or acquired
-Impaired: failure in recognizing faces (even own family)
-Spared: recognition by voice, clothes and making associations, able to match different views of faces and name other objects
-Evidence for faces being special