Neuropsychology: The Seeing Brain Flashcards
What kind of process is seeing?
-Complex (hierarchical) process
-Constructive process
-Example: Kanisza illusion
How is seeing a complex process?
-Eyes and brain play important roles
-Psychological and cognitive models: how does visual perception happen and which processes are involved
How is seeing a constructive process?
Things are added to input and interpreted in certain way
What is the Kanizsa illusion?
-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
What is the hierarchical system of seeing?
-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)
What are characteristics of the retina?
-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
What are rod cells?
-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
What are cone cells?
-In retina of eye
-Specialized for detecting different wavelengths of light
-More active during day time
-Highest concentration in fovea
What is the geniculostriate pathway?
-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
Which route does the geniculostriate pathway follow?
-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
What kinds of conditions can be the result of damage somewhere in the geniculostriate pathway?
-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
What are characteristics of the lateral geniculate nucleus (LGN)?
-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
What are characteristics of the primary visual cortex (V1, striate cortex)?
-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
What are the stages of cells in the primary visual cortex according to Hubel & Wiesel?
-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
Which types of cells can be found in the primary visual cortex (V1)?
-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
What is retinotopic organisation?
-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)
What kind of blindness can be the result of damage to parts of the primary visual cortex?
-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
Why is the place of damage important?
-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
What are the consequences of the geniculostriate pathway being the most important for conscious vision?
-Damage to pathway impairs conscious vision
-But other aspects spared
-Example: blindsight
What is blindsight?
-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)
What are characteristics of blindsight?
-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
What other regions are involved in seeing?
-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
What is the V4 area?
-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
Why does the brain need a specialized processing system for color, while the retina is already sensitive to different wavelengths of light?
-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
What is achromatopsia?
-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
What is the V5/MT area?
-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
What is biological motion?
-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
What is akinetopsia?
-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
What is needed beyond the visual cortex to see?
-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
How is all the visual info put together to form a coherent perception according to the model of object recognition?
-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)
What consequences can damage in different stages of model of object recognition have?
-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
What is visual agnosia?
-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)
What is apperceptive agnosia?
-Type of visual agnosia
-Disorder in forming coherent visual representation
-2 types: integrative and visual form agnosia
What is associative agnosia?
-Type of visual agnosia
-Disorder in recognition and linking despite intact visual representation
Which Gestalt principles are there to combine parts into a whole?
-Law of proximity
-Law of similarity
-Law of good continuation
-Law of closure
What is integrative agnosia?
-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
What is visual form agnosia?
-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)
What is object constancy?
-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
What are the neural substrates of object constancy?
-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
What is object orientation agnosia?
-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
Which areas in the higher ventral vision pathway are associated with different object categories?
-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
What is special about faces?
-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
Which different aspects of face processing did Bruce & Young find (1986)?
-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)
What kind of evidence is there for the Bruce & Young model of processing faces?
-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
What brain regions were connected to different processes of face recognition by Haxby et al. (2000)?
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)
What is prosopagnosia?
-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
