Week 9 The Visual System Flashcards

1
Q

Vision tings

A
  • Far sense – light travels fast ~300,000km/sec
  • Stimulus is EM energy – light source is usually the sun
  • Allows us to identify, locate and react to things in the environment; allows
    communication
  • Process of inverse optics – emitted light itself seldom the message of interest, the
    reflection of light off objects is more relevant
    o When light hits an object, some of it is absorbed and some is reflected
  • Amount of light reflected
    o Off an object gives us a perception of lightness
  • Pattern of light reflected
    o Gives us a perception of shape, texture
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2
Q

Stimulus for vision

A
  • Electromagnetic energy within the visible spectrum
  • Stimulus properties
    o Intensity
  • Perceptual submodalities
    o Intensity – gives brightness
    o Wavelength – gives perception of colour
     Visible spectrum – nM ~ 400-750nM
  • Measure
    o Watt/m^2 or lumen/W or candelas/m^2
    o Log scales because expanded stimulus::intensity relationship
  • Property of object
    o Reflected light = lightness measured in candelas
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3
Q

The human eye

A
  • 3 layers
    o Fibrous tunic
     Protection and shape – sclera (white of eye)
     Anterior portion is thinner (cornea) – helps refract light
    o Vascular tunic
     Vascular nourishment
     Pigmentation reduces light scatter – pigment determines eye colour
     Manufactures aqueous humour by ciliary body
    o Retina
     Stimulus detection and signal transduction
     Where sensory neurons are located
  • 2 chambers
    o Anterior chamber
     Filled with aqueous humour made by ciliary bodies
     Pressure is important – ciliary bodies continually making liquid, filling up – need to drain the old fluid via ducts
     If pressure builds up it creates pain in the eye, pushing on the lens and optic nerve
     Glaucoma – imbalance in pressure
     Can permanently damage eye
    o Vitreous chamber
     Filled with vitreous fluid
     Can see when stuff gets built up in it
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4
Q

Puplis

A
  • Can accommodate (dilate, constrict) to alter amount of light entering eye
    o Bright – gets smaller
    o Dark – bigger
  • Influenced by
    o Light levels
    o Autonomic nervous system
     Sympathetic nervous system – gets bigger to potentially see anything in environment to be ready for
     Parasympathetic – gets smaller, less likely to be something in enviro you need to respond to
     Emotional state
     Shows in pupils
     Paying attention, excited, romantic
    o Drugs
     Opioids – tiny pupils, impaired vision
     Cholinergic – dilate
    o Age
     As you get older you lose pupillary accommodation ability
     Change is smaller vs young people
     Lose ability – contributor towards presbyopia
     Sight of old age
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5
Q

Presbyopia

A
  • Sight of old age
  • Lose pupillary accommodation
    o Things look darker – turn on all the lights
  • Lose lens accommodation
    o Things become out of focus
  • Increase in lens thickness
    o Things become blurry, out of focus
    o Reduced visual acuity
  • Lose spatial packing of rods and cones
    o Become more spread out as you age
    o Lose visual acuity
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6
Q

Visual Focus

A
  • The optics of the eye function to refract waves of light onto retina
    o Cornea provides initial refraction
     Shape of cornea must be correct to get right refraction
     Can reshape cornea to bend light in a different manner to improve vision
    o Lens provides further refraction, ciliary muscles control accommodation
     Muscles alter shape of lens, pull it taught or make it fatter – contract and relax to accommodate
  • Need to bend the light for maximum visual acuity
    o Bends through cornea and again through lens so the light converges on the fovea to have the sharpest resolution vision we can have
  • In addition to refraction
    o The eyeball must be the right shape and size so the focused image falls onto the retina exactly
    o Eyeball needs to be the right length for the optics of the eye you’re born with
     If born with optical power from cornea and lens of a set amount, that doesn’t match eyeball shape, you might be near sighted or far sighted
     Eyeball too long – vision point of focus falls before fovea
     Eyeball too short – focus falls behind fovea
    o Put contact lens in front of eye to shape the refraction so it falls on the right part of the eyeball
  • Lens accommodation decreases with age
    o Second contributor to presbyopia
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7
Q

Lens

A
  • Can accommodate (make more or less convex) to improve refraction of light
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8
Q

Lens transparency is essential

A

o Reduced transparency = cataract
 Cumulative UV exposure – lens acts as filter to protect from UV, can
be damaged and lead to cataract – wear sunglasses
 Congenital – detrimental to visual cortex development
 Needs to be removed or visual pathways doesn’t develop fully o Cataract lens can be surgically removed
 Compensate with strong optical spectacles or replace with synthetic lens
 Refraction power of lens can be replaced, but accommodation lost

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9
Q

When lens is taken out

A

o Some people start to have capabilities in UV light
o Usually UV is outside of visible spectrum – if take lens out, people can start to see UV, adds additional spectrum
o Things have glows to them – neural wise, brain has inbuilt capabilities to see UV light, but don’t see it as lens blocks it from entering eye

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10
Q

The lens grows all throughout your life

A

o From age 0-90, there is !4x increase in thickness
o Third contributor to presbyopia
o Reduced visual acuity
o Things become blurry – also because of lost accommodation
o Need glasses to assist

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11
Q

Retina

A
  • Two odd features
    o Photoreceptors are located at the back of the retina
    o Light decreases the amount of neurotransmitter release
     There is baseline level of NT release from photoreceptors, when light hits them, it reduces or stops sending NT out
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12
Q

Retina

2 subtypes

A

o Rods
 Peak absorption at ~500nm
 Activated between 400-600nm
 Very sensitive – can be activated by 1 photon
 Low acuity – rough, pixilated vision
 Key for night/scotopic vision
 Allows to see little specs of light
 Key for peripheral vision
o Cones
 Peak at !440, 530, 560nm
 Have different spectrums
 Less sensitive – need 100+ photons to activate
 High acuity
 Key for high-res colour/photopic vision
 Concentrated in macula and fovea
- Best visual acuity in the macula, worst acuity (no acuity) in the blind spot
o Where axons of retinal ganglion cells exit the eye at the optic disk

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13
Q

Dark adaptation

A
  • You can gain activity in scotopic vision if you are patient
    o Can make rods higher acuity if you give them more time in dark environment
  • Any exposure to light breaks the dark adaptation of the rods – sudden return to poor
    acuity
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14
Q

Cones

dark adaptation

A

o Absolute threshold – minimum light needed to activate
o Start at say 75 and drop to about 50 – need 50 photons of light to activate the cones still
 Won’t drop more than that – if less then 50 they won’t activate at all – will think it is dark there

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15
Q

Rods (dark adaptation)

A

o As you spend more time in the dark the absolute threshold drops
o To a point where minimal amounts of light will be detected – sensitivity increases
o Can see in a room that was initially pitch black
o Any bit of light in the room will break the adaptation
 Go back to reliant on cones
 Except one form of light

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16
Q

Long wave light

A

o Red spectrum light
 rods are not activated by EM energy that is >650nm (red)
o if these wavelengths are the only ones in your environment; only getting red light
 cones detect the presence of this energy and allow you to see
 Rods don’t detect this energy – they go into adaptation mode and
prep you for scotopic vision
 Cycle of dark adaptation occurs and get rod sensitivity
o Uses
 Training who need to go out in the dark in red light conditions
 Fighter pilots need to be able to fly at night
o Red spectrum light
 rods are not activated by EM energy that is >650nm (red)
o if these wavelengths are the only ones in your environment; only getting red light
 cones detect the presence of this energy and allow you to see
 Rods don’t detect this energy – they go into adaptation mode and
prep you for scotopic vision
 Cycle of dark adaptation occurs and get rod sensitivity
o Uses
 Training who need to go out in the dark in red light conditions
 Fighter pilots need to be able to fly at night
 Sit in a red lit room – rods accommodate but cones still see
 Eyes are ready to see in the dark if called to fly

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17
Q

Oguchi’s disease

Deficits in dark adaptation

A

 Rare disorder where rod adaptation takes 3-4 hours
 Conformational change is slow
 Get impaired night vision, delayed scotopic vision

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18
Q

Retinitis pigmentosa

Deficits in dark adaptation

A

 Eye disorder associated with genetic aetiology
 Lose visual acuity – dying cells
 Rods are initial victims – first to die off
 Impaired night vision and peripheral vision
 Lose two facets dependent on rod function
 Visual scene gets tunnel vision – progressively until can only see in
macula
 Eventually cones die off as well – completely blind

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19
Q

Variations in retina

A
  • Rod/cone distribution
    o Cones are concentrated in macula
    o Macula appears dark on scan thing because of concentration
  • Thickness
    o Thinnest in specific region of macula – fovea
    o Foveal pit
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20
Q

Spatial arrangement of rods/cones

A

o For best acuity, photoreceptors need to be tightly packed in an ordered fashion
o If not packed – spaces in a loose arrangement
 You get low resolution vision
 Diffuse looking scenes
 Pixilated almost, depending on how diffuse arrangement is
o Spatially diffuse in infancy, mature in 4 years, decline with age
 Rods and cones lose spatial packing – get more spread out as you age
 4th contributor to presbyopia
o Albinism exhibits permanent spatially diffuse photoreceptors
 Lack melanin – pigment in tunic later that helps light scatter
 Lack light scatter
 Rods and cones never become tightly packed also – things stay
pixilated from childhood

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21
Q

Photoreceptor distribution

A
  • Cones highest in fovea region of macula - give macula highest acuity for vision
  • Macular degeneration most common cause of blindness over 50 years of age
    o Lose central visual field and start to get scotoma in centre of field
    o Absence of visual scene, lack of info
    o Blind spot that follows where you’re trying to focus on
    o Shifts with eyes
    o Gets bigger
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22
Q

Blind spot

A
  • Edme mariotte in dissection noticed variation in retina at site of optic disk
    o No photoreceptors on this spot
  • Filling in perceptual completion demonstrated by Wallis, and Ramachandran
    o Simple patterns/textures/background are filled in
    o Don’t notice the spot
    o Complex items are not filled in
    o Illustrates top-down educated guesswork of brain
     Use info you have, to make a guess – can only make inference so far
     Can’t fill in a table or a face but can fill in pattern on a wall or floor  Fill it in with whatever is around it
    o Enables smooth, stable perception despite constant interruption in the incoming signal
     Perceptual stability – gaps in incoming signal but don’t perceive them
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23
Q

Perceptual stability

A
  • Frequent changes/gaps in sensory stimuli are not perceived due to compensatory
    neural mechanisms; perception remains stable/unchanged
  • Examples
    o VOR
    o Blind spot filling
    o Blink suppression
24
Q

Blinks

A
  • Clean and moisten the eye, reflexively protect
  • Involuntary or voluntary
  • Blink rates indicate interest/attention, increase during social interaction
  • Last about 1/3 of a second
    o For half this time eyes are completely closed
    o We don’t experience brief blackouts every time we blink
     Not filling in
  • Brain is suppressing visual processing before each blink
     It knows blink is coming – compensatory mechanism
     So that you don’t perceive the interruption in info
25
Q

Process of vision

A
  • 3 part relay – trisynaptic
  • Convergence of info
    o Start with ~127 million photoreceptor cells converging to 1.25 million ganglion cells
    o Much fewer ganglion
    o Send somewhat already processed signal to brain
    1. Electromagnetic energy hits photoreceptor cell
    o Signal transduction
    o Horizontal cell – signal to noise amplification
    2. Bipolar cells detect the change in neural signal
    o Relays signal to ganglion cells
    o 2 types of bipolar – increment responsive and decrement responsive
    o Amacrine cells – signal to noise amplification
    3. Ganglion cells send signal to brain
    o Via CNII
26
Q

Ganglion cells

A
  • Each shows a receptive field for a specific region of space in the visual field
  • Single unit recording (1 fibre of optic nerve = 1 axon of 1 ganglion cell)
    o In dark, AP still being recorded – baseline activity
    o In lit room, as the stimulus moves across the screen, APs increase in one part of the grid and decrease in other parts
27
Q

Centre surround receptive fields

A

o Some are on centre – when light is in the centre the cell firing increases
 For optimal FR – light in centre, dark in surround
 Cell firing decreases when light in surround
 Cell firing stays at baseline at most other times
 If light everywhere it cancels out – increase activity but simultaneously decrease activity so net result is 0
o Some are off centre – when light is in the centre the cell decreases firing
 For optimal FR – light in surround, dark in centre
o Vision need changes in light, edges, differences in light and dark

28
Q

Ganglion receptive fields

A

o The centre and surround work in an antagonistic manner

o Optimal FR changes occur only when circumscribed light/dark regions detected

29
Q

Data processing in the retina

A

o Photoreceptor cells provide raw data on light levels in visual field
o The raw data is overwhelming and not that useful/informative by itself
o What is useful/informative is where significant differences occur in that data
 More efficient if info going to brain has already been processed a bit
 Want to know differences, not similarities – where receptive field
picks up a higher level and lower in surround
 A change occurs here
 Ganglion cells send info when there is a change
 Figure out where differences lie
 Helps to find edges and boarders – allow to distinguish thing in visual field
o Ganglion cells work to collate the photoreceptor data
 127 mil bits of data - 1.2 mil ‘results’
o What we’re really interested in is differences in light levels within that visual field
 Edges/boards/contrast - shapes - features
 Centre surround processing helps pick up edges of objects instantaneously

30
Q

Basic visual processing

A
  1. Process of vision
  2. Retinal relay
    o Photoreceptor-bipolar-ganglion
  3. Neural signal travels along CNII
    o Rearrangement at optic chiasm
  4. 20% signals sent to superior colliculus – midbrain
    o Old visual pathway
    o Responsive to sudden shifts in light
    o Serves to orient head/eyes to visual stimuli
    o Shift attention and movement of eyes to sudden changes in visual environment
    o SC connects to muscles that controls eyes
    o Respond to sudden changes – can detect and shift attention
    - 80% of signals sent to lateral geniculate nuclei –thalamus
    o The LGN has distinct layers, each containing a retinotopic map
    o Spatial arrangement from retina maintained
  5. Signal sent to V1 primary visual cortex
    o Retinotopic map maintained – left V1 receives info from right visual field (L+R eyes) and vice versa
31
Q

Visual cortex key features

A
  • Retinotopic maps maintained in V1
  • Hierarchical processing
    o Starts with basic info sent from V1-V2 etc to add on more complexity of info, building from bottom up
  • Concurrent processing
    o V1-V2-V3 etc.
    o Send info up hierarchy and at each step send info back that modulates further incoming signals going up
    o V1 also sends projections back to LGN thalamus
     Circular processing
32
Q

Visual processing

A
  • Visual processing occurs along two streams:
  • Ventral ‘what’ stream
    o What we are looking at – object perception, colour perception
  • Dorsal ‘where/how’ stream
    o Spatial – how is movement integrated
33
Q

Damage to V1

A

o Blindsight
 Can’t perceive what is in blind hemifield but can identify where an object is
 Unconscious sight
o Old SC pathway still active – up to dorsal stream
 Helps you orient and gives conscious perception of where things are in the environment
 Not necessarily attending to them but still processing

34
Q

David Hubel and Torsten Wiesel

Feature detection in V1

A

o Shone light across visual field of cat – recordings along visual pathway
o Centre surround firing responses in ganglion cells and LGN thalamus
 Ganglion cells have a bigger centre surround
o V1 cells didn’t respond to patterns of light moving across
 Nothing worked – different shapes
 Accidentally left recording on during slide switching
 Cell fired to switching of slide
 Respond to movement going downward but not back up

35
Q

Cells in V1

Feature detection in V1

A

o Found that V1 cortical cells show specific responses to specific stimuli
 V1 cells exhibit feature detection o Some cells exhibit e.g.
 Ocular dominance
 They respond more strongly to stimulation in the left eye vs
the right eye or vice versa
 Orientation selectivity
 They respond more strongly to horizontal bar stimuli or vertical
bar stimuli
 Direction selectivity
 They respond more strongly to moving stimuli left or right or
vice versa, or up to down or vice versa
 Any many other forms of selectivity

36
Q

V1 cortical development

Feature detection in V1

A

o Feature detection in V1 is influenced by experience
 Experience dependent plasticity e.g. monocular deprivation, selective rearing
o Proper V1 development required visual input early on in life – critical phase
 Multiple facets of vision mean multiple critical phases
 Some critical phases for anatomy, some for functionality
 Have to have experience in first few months of life of those features so the V1 cells become specific for feature detection
 Don’t get exposure in critical time – won’t develop feature
detectors for what was lacking in environment
o Need visual experience, exposure
o Deficits in the eye or early visual pathway in infancy can impair proper develop of V1
 Lazy eye – one eye doesn’t have as much acuity
 Recognise one eye is weak and correct with glasses early on to teach weak eye to get visual input so hemifield develops

37
Q

V1 vision – a Cezanne painting

A
  • V1 provides feature detection but this is not vision as we know it
    o V1 cells are very basic things
    o How do we take orientation and movement and lines and perceive objects and people and landscapes instantaneously?
  • Feature detection
    o Edges, boarders, contrast, shading
    o In black and white
38
Q

How do we add colour

A

o Incoming signal from retina contains coded info that relates to nM differences in the surrounding EM energy
 Tri- di- monochromatic codes
 Dichromatic – colour blind, see different colour spectrum
 Mono – black and white
o V1-V2-V4
 V2 – contrast, contour, shading
 V4 – decodes colour message
o V4 is needed to translate this code into a colour qualia
 Things become recognisable – can make assumptions about what
you’re looking at

39
Q

Damage to V4

A

o Cerebral achromatopsia = cortical colour blindness
o Without colour vision at cerebral level – lost ability to decode colour
messages

40
Q

How do we recognise objects

A

o Can make assumption about what you’re seeing based on colour
 Can detect colour differences to find things – can find bananas, tell if they are rotten or ripe

41
Q

Object perception

Bottom up

A
  • Light detection-edge detection-feature detection-object discrimination- ? -
    object identification
  • Bottom up?
    o Pattern recognition
    o Do we put together all the basic elements/features/geons and recognise the pattern
     Pattern X = object X
     Take all the things and add together into a full object
    o Pro?
     Logical – fits physiology and idea of hierarchical processing
     Putting increasingly complex things together to build the whole object
    o AI robot vision
     Our current best hope for developing robotic vision
     Getting from discrimination to identification – what is the step in
    between?
     Lack of AI visual perception
    o Con
     Doesn’t account for speed of object perception
     Don’t have to build the stages of what we’re seeing
     We process very fast, if we had to build things up each time it
    would not be this quick
42
Q

Object perception

Top Down

A

o Theories for pattern recognition:
 Brain formulates constant hypotheses about patterns present in environment
 (stemming from experience)
 Makes an educated guess
 Then checks essential details to confirm
o Would allow for rapid, efficient object perception
 By allowing us to skip some of the tedious steps of visual data
processing
 Haven’t processed every bit of info but can still see the scene
 Allows fast and fluid perception
o In many instances we do seem to skip over the precise visual data
 Perceptual set processing
 Have a hypothesis already, check minor details, move on very
fast
 Make a guess about what the word is based on first and last
letter
 Can make sense of muddled information
 Don’t pay attention to your own mistakes as you know what
you’re trying to say – other people can see them
 Inverted face phenomenon
 Eyes and mouth in wrong positions
 Everything askew in actual sensory info but you don’t perceive it
o Skipping over data
 We have coherent visual percepts even if the exact sensory stimuli are:
 Missing/wrong/ambiguous
 Different in different situation
o Size constancy
 Interpretation is solid even if size is different
 Have understanding based on knowledge of depth perception that a person far away is a normal sized human
o Shape constancy
 Turn an object to profile – know that when
things turn the shape goes linear
 Skip over visual data and have a coherent recognition even if things are wrong within visual scene
 This suggests there is a strong top down influence on vision

43
Q

Object perception

Inference

A

o Based on previous knowledge gained through a lifetime of experience, we can make a best guess and this enables rapid visual perception
o Most of our reality is our brain’s best guess
 As long as it is close enough not to impact our survival it lets us function in the world
 Allows fluid functioning

44
Q

Object perception

AI

A

o Robots lack this part of perception
o Top down processing is hard to build
 How to give them knowledge base
 Need every single object in every shape and size and with obscurities
o Let them learn these things
 Play with things, pull them apart, move them around
 Integrate with motor robotics to learn perceptual tactics
o Merging motor and AI
 Have to learn all these things throughout lifetime
 Build a baby robot and teach from infancy about perceptual world

45
Q

Motion perception

A
  • How do we add motion? Especially complex motion
    oSuperior colliculus-dorsal visual stream gives some info
    o V1 feature detection gives some info
    o V1-V2-V5/MT
     V5 is needed to bind feature motion into global motion
     STS – biological motion
46
Q

Damage to V5

A

o Lack fluid motion perception
o Can’t see movement in environment
 See frames – brain updates position of things but can’t see the movement

47
Q

Motion + Biological motion

A
  1. Motion
    o Is there something moving in our visual scene
    o The pattern of motion helps with recognition
    o V5/MT
  2. Biological motion
    o Is there something animate moving in our visual scene
    o Is it alive vs a tree
    o The pattern of motion helps with recognition
    o What is the critical components of the pattern: limb movement
    o Superior temporal sulcus STS
48
Q

Biological motion

A
  • Recognising movement as animate/alive vs inanimate
  • Point light motion experiments
    o Stationary frames difficult to comprehend, but joint based motion almost immediately enhances our perceptual understanding of biological motion
     STS activation
    o Can even discriminate identity, gender, emotion in dancing point light
    participants
    o Attention to biological motion develops ~4months, and does not decline with age
     Inter-species characteristic
  • Applications
    o Motion capture tech and facial capture tech for actors
     Makes the movie seem more real
     Lights up STS – it is moving how a human would move
49
Q

Eyes in constant motion

A
  • Yet we don’t perceive constant motion
  • Our eyes are moving
    o When we move, our eyes move with our body
     Visual scene stays still
     VOR
    o When we turn our head fast our eyes move fast
     We don’t see a blur in visual field
     VOR
    o When we dart our eyes around to read/drive/watch TV
     We don’t see motion
     Saccades, not VOR
50
Q

Saccades

A

o Rapid eye movements that occur between visual fixation points
o Our eyes saccade around a scene – looking at a face we look everywhere
 We don’t see motion
- Why don’t we experience blurred vision during saccades?
o Maybe they are too past to perceive ?
 Saccadic movements ~20cm/sec – quite slow
 But we can detect fast things
o Maybe brain suppresses visual shift when due to a saccade
 Motion sensitive cells in MT are silenced during saccades suggests
brain monitors self-induced shifts in visual field

51
Q

Saccadic suppression

A

o Gives you perceptual stability
o You don’t see the motion, sudden changes in stimuli are not perceived due to V5/MT suppression
o Motion perception suppressed

52
Q

Examples of perceptual stability

A
  • VOR
  • Blind spot filling in
  • Blink suppression
  • Saccadic suppression
53
Q

Driving and visual perception

A
  • Driving itself is a massive feat of visual and sensori-motor integration
  • Self-driving cars
    o Can’t build a car that has the function of human visual perception
    o Can’t tell the difference between a cat and a leaf
  • Driving involves a lot of visual motion processing
    o Constant saccades to scan scene
    o Tracking to track cars/pedestrians
    o Calculating distances, speeds, ect.
    o Predicting changes in distance, speed, etc.
  • Alcohol
    o Slows initiation and velocity of saccades
    o Impedes tracking
    o The brain tries to catch up by initiating fast saccades = jerky eye movements
     Perceptual instability
    o Not only is your motor response time impaired but your ability to visually detect events in the first place is impaired
54
Q

Case Studies One

A

o Deets
 79, male
 Age related macular degeneration, early cataracts, significant vision loss
 For last 6 months vivid hallucinations in scotomas
 Road maps, wreaths, faces
 Acknowledges not real – finds amusing
o Evaluative tests
 Visual acuity – vision 20/400 and 20/200
 Macular degeneration
 CT scan fine
 MMSE 23/29
 No drugs other than prescription
o Diagnosis
 Charles Bonnet Syndrome
 Damage to any part along the visual pathway can lead to abnormal region of blindness in the visual field = scotoma
 Levels of scotoma depend on where damage is in the pathway
 Can have hallucinations populate tunnel vision as well – just
not CBS
 Specific type of hallucination
 Visual hallucination in established scotoma
 A release hallucination – a response to sensory deprivation
 Lose input – those neurons become unmasked, released
o Baseline levels no longer suppressed
 When the brain doesn’t get sensory activity is starts to make its own
 Wants input to come up to a normal level
 Give yourself a perceptual world
 Endogenously – complex hallucinations

55
Q

Case Studies Two

A

o Deets
 38, male
 Over last 8 months, episodes of macropsia and micropsia, including lilliputianism
 Changes in shapes and sizes of objects, traces of objects left even after it is gone
 More noticeable during stressful weeks at work, starting to impair function at worl
 Acknowledges not real – but unnerving
 Initially said this was recent but admitted it has been
happening for years
o Evaluative tests
 Visual acuity – 20/30 and 20/20
 Normal ophthalmic exam
 CT scan fine
 MMSE 29/30
 Drug trace – alcohol and cannabis
o Diagnosis
 Alice in wonderland syndrome
 Transient alteration in visual object perception due to transient
changes in neural processing
 Micropsia and macropsia – illusion/distortions
 In the sensory cortices, changes in neuronal activity and neural processing can alter S&P
 Alterations could be caused by
 Migraine SD, epilepsy
o Hyperactivity in brain regions
 Neuronal injury
o Lose perceptual capacity
 Neurdegeneration
 Electrical stimulation
o Make neurons active to cause perception
 Drugs
o Heaps of drugs can cause alteration in S&P particularly at high doses, but only one drugs class does this intentionally – psychedelics

56
Q

Week 9 The Visual System

A