Week 9 The Visual System Flashcards
Vision tings
- 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
Stimulus for vision
- 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
The human eye
- 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
Puplis
- 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
Presbyopia
- 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
Visual Focus
- 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
Lens
- Can accommodate (make more or less convex) to improve refraction of light
Lens transparency is essential
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
When lens is taken out
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
The lens grows all throughout your life
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
Retina
- 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
Retina
2 subtypes
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
Dark adaptation
- 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
Cones
dark adaptation
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
Rods (dark adaptation)
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
Long wave light
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
Oguchi’s disease
Deficits in dark adaptation
Rare disorder where rod adaptation takes 3-4 hours
Conformational change is slow
Get impaired night vision, delayed scotopic vision
Retinitis pigmentosa
Deficits in dark adaptation
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
Variations in retina
- 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
Spatial arrangement of rods/cones
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
Photoreceptor distribution
- 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
Blind spot
- 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
Perceptual stability
- 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
Blinks
- 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
Process of vision
- 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
Ganglion cells
- 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
Centre surround receptive fields
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
Ganglion receptive fields
o The centre and surround work in an antagonistic manner
o Optimal FR changes occur only when circumscribed light/dark regions detected
Data processing in the retina
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
Basic visual processing
- Process of vision
- Retinal relay
o Photoreceptor-bipolar-ganglion - Neural signal travels along CNII
o Rearrangement at optic chiasm - 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 - 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
Visual cortex key features
- 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
Visual processing
- 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
Damage to V1
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
David Hubel and Torsten Wiesel
Feature detection in V1
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
Cells in V1
Feature detection in V1
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
V1 cortical development
Feature detection in V1
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
V1 vision – a Cezanne painting
- 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
How do we add colour
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
Damage to V4
o Cerebral achromatopsia = cortical colour blindness
o Without colour vision at cerebral level – lost ability to decode colour
messages
How do we recognise objects
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
Object perception
Bottom up
- 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
Object perception
Top Down
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
Object perception
Inference
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
Object perception
AI
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
Motion perception
- 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
Damage to V5
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
Motion + Biological motion
- Motion
o Is there something moving in our visual scene
o The pattern of motion helps with recognition
o V5/MT - 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
Biological motion
- 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
Eyes in constant motion
- 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
Saccades
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
Saccadic suppression
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
Examples of perceptual stability
- VOR
- Blind spot filling in
- Blink suppression
- Saccadic suppression
Driving and visual perception
- 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
Case Studies One
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
Case Studies Two
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
Week 9 The Visual System
