1
Q
Who was patient TN?
A
- Strokes caused damage to visual cortex in both hemispheres
- TN reports being totally ‘blind’
- Uncanny Sight in the Blind
- Scientific American, May 2010.
- “You can experience a total loss of your cortical vision but still retain some capacity to move around inside and out without damage to yourself”
- de Gelder, B. (2010)
2
Q
What is blindsight?
A
- “Visual discrimination in the absence of acknowledged awareness” –Weiskrantz (1990)
- Early description by Riddoch (1917)
- Working with brain damaged soldiers in WWI
- Noticed patients’ ability to detect motion in an otherwise blind visual field
- Term ‘blindsight’ first used by Sanders et al. (1974)
- Blind man being able to find his way around a maze with obstacles
- Ability to allow you to see although you’re blind
- Ability to detect things in the environment without being aware of seeing them
3
Q
How can you test blindsight?
A
- Stimulus moving either horizontally or vertically
- Cannot see the stimulus itself, e.g. colour, shape
4
Q
What is blindsight and hindsight?
A
- The term ‘blindsight’ came from the title of a talk by Larry Weiskrantz:
- “Blindsightand hindsight”
- Blindsight–refers to behavioural findings
- Hindsight –implies role of the hindbrain and subcortical visual pathways
- Hindbrain is the oldest part of the brain in evolutionary terms – need them for survival, located where the spinal cord and brain meet
5
Q
What is in the hindbrain?
A
- Medulla
- Cerebellum
- Pons
- Reticular formation
6
Q
What did Weiskrantz – The Ferrier Lecture 1989 -Proceedings of Royal Society (1990) lead to what we know now about visual functions?
A
- We know a lot about about visual functions
- We now know that functions are localised in cortex.
- Main pathway from eye to visual cortex
- Geniculo-striate pathway (90%)
- one million nerve fibres
- Smaller sub cortical pathway (10%)
- 150,000 nerves
7
Q
What is the main pathway from the eye to the visual cortex?
A
- Anterior (before) and Posterior pathways (after)
- Sensory inputs -Primary visual cortex (V1) and striate cortex
- Extrastriate areas consist of V2, V3, V4,V5
8
Q
Functions of visual cortex: Species differences
A
- It has been proposed that animals’ visual abilities can survive damage to visual cortex while humans’ visual abilities cannot
- Studies of blindsight arose primarily from comparing the effects of damage to visual cortex in man and monkey
- For example: there has been evidence than the removal of the occipital lobe in monkeys does not cause blindness
- Not the case in humans – can cause blindness if occipital lobe is damaged
9
Q
Monkeys without primary visual cortex can:
A
- discriminate shapes
- maintain (reduced) acuity
- fixate and reach towards small and brief visual events
- detect movement
- Humans typically function blind
10
Q
What is -Cortical blindness ?
A
Loss of vision following damage to visual cortex (e.g. area V1, not the retina or optic tract)
11
Q
What is -Hemianopia ?
A
Loss of vision in one half of visual field following unilateral brain damage
12
Q
How does information flow from retina to cortex?
A
- Information comes in through the eye and travels to Primary visual cortex via the lateral gen
- Goes to higher areas for visual processing
13
Q
‘What’ and ‘where’ visual pathways (Mishkin & Ungerleider, 1982)
A
- ‘What’ (How) pathway (ventral stream) – processes object recognition and identification
- ‘Where’ pathway (dorsal stream) -spatial perception, where the object is located
- Two pathways run parallel to each other
14
Q
Measures of blindsight?
A
- Detection of stimuli in blind hemifield
- Discrimination of stimuli in blind hemifield
- Implicit influences of stimuli in blind hemifield
- On reaction times
- On eye movements
15
Q
The first experimental demonstration of blindsight in humans was?
A
- Poppel, Held and Frost (1973)
- Four patients with visual field defects following unilateral brain damage
- Visual stimuli projected at different locations in their blind visual field
- Patients asked to move their eyes to the position of the stimuli (auditory ‘go’ signal).
- Patients were puzzled by the task: “How can I move my eyes to something I haven’t seen?”
16
Q
Who was patient DB?
A
- Weiskrantz et al (1974)
- Patient DB - 34 year old male at time of brain damage
- Surgical removal of tumour in right occipital lobe (severe migraine attacks)
- Resulted in a left hemianopia
- One of the most studied blindsight cases
- Could guess the properties of the stimulus
17
Q
What experiment was conducted on patient DB?
A
1 Experimental condition: Light flashed at one of 7 locations in blind hemi-field, followed by an auditory tone
2 Control condition: target location not illuminated (auditory tone is still presented)
3 Both conditions: DB asked to move his eyes to the target location on hearing the tone, or to point to the location
18
Q
How did DB perform in the experiment?
A
- Replicates the results of Pöppelet al. (1973)
- Much higher spatial accuracy for pointing movements than eye movements
- Weak correspondence between target position
- High spatial accuracy
19
Q
How did DB react to his performance?
A
- DB was ‘openly astonished’ when shown video of his reaching performance
- Claimed to have ‘seen’ nothing at all in blind field
- When ‘blank’ trials inserted DB had a vague feeling that stimuli not always presented
20
Q
Who was patient GD?
A
- Patient GD
- Reaction times are faster when two targets are present than when only one is present
- Is this effect seen when the additional target appears in the blind field?
- Yes (but only for some patients…)
21
Q
Further demonstration in 2 out of 4 cases?
A
- Corbetta et al (1990)
- S = single light in good hemifield
- D1 = Two lights good hemifield
- D2 = Lights in good and blind hemifields
- A) group mean – not significant
- B) Case 2 shows a ‘spatial summation’ facilitation effect
22
Q
What did Rafal et al (1990) do showing lights and hemifields?
A
- Showed a light only in the good hemifield
- Task -move eyes to light in good field (monocular viewing)
- Eye movements (saccades) were slowed by the presence of distractors in the blind field
- Must be processing in the blind field
23
Q
Implicit measures: Galvanic skin response (GSR)
A
- Skin conductance – measures changes in the skin
- Reflects physiological arousal to a stimulus
- Not under conscious control modulated by sympathetic nervous system
- So, damage to visual cortex does not abolish response to light in blindfield
- The response shows visual processing still occurs and it does not depend on recognition of the stimulus
- GSR – reflects registration of a stimulus
24
Q
Implicit measures: Pupil response?
A
- Constriction (narrowing of the pupil – increased light) and dilation (increase of pupil – used in fight or flight)
- Depends on light level and indicates person’s interest and arousal
- Pupil response is also sensitive to:
- Spatial frequency (measure of visual acuity) – high detail such as facial features
- Low spatial frequency – low detail such as a blurred image
- Cognitive load
25
Pupillary reflex: circuit ?
- Back of the eye is a retina, which needs to communicate with the brain. Uses optic nerves
- Retina and optic nerve send projections to pretectal regions in the midbrain (Subcortical)
- Pretectal nucleus, lateral geniculate nucleus, endinger Westphal nucleus
- Pretectal signals sent to ciliary nerve controls the ciliary sphincter
- Pupil dilation: decrease in light Fight-or-flight response
- Constriction: Increase in light
- Visual acuity – spatial resolving capacity of the visual system
- How well we see fine detail Spatial resolution Measured with ‘gratings’
- Spatial frequency of the grating
26
Pupil response and patient GY
- Responds after cortical damage
- GY –pupil response modulated by ‘spatial frequency’ in blindfield
- Pupil response from: GY (human) and two lesioned monkeys (Cowey, (2004)
- Pupils were able to respond to visual stimuli – constricting and dilating
27
What is residual vision and what different routes have been associated with blindsight?
- Some remaining visual functioning in the main (geniculostriate) visual pathway
- Small areas of vision which are still functioning
- Blindsight has been attributed to three different routes (hypothesis)
1. Extrageniculate activity – from the subcortical pathways
2. Geniculo-extrastriate
3. Visual cortex sparing
28
Can blindsight be attributed to residual vision?
- Blindsight cases, like DB, may have small regions of intact (residual) vision
- Light from stimulus may have reached these small regions of spared vision, enabling the observed ‘blindsight’ behaviour
29
What did Fendrich, Wessinger and Gazzaniga (1992) find with a patient diagnosed with complete hemianopia?
- Fendrich, Wessinger and Gazzaniga (1992) patient diagnosed with complete hemianopia finer testing methods identified regions of intact vision (‘islands’)
- However, other cases have been reported following complete loss of V1 as confirmed by MRI Bridge et al. (2008)
30
Who is patient GY?
- Brain damage restricted to primary visual cortex (V1) Aged 8 years
- Right hemianopia
- Didn’t show activation in the V1, but in the extra striate areas
- Barburet al. (1988)
- GY made highly accurate eye movements to stimuli in his blind field
- Moreland et al (2004) –patient GY (no activation striate cortex) and patient RA (activation of calcarine sulcus)
- GY was not aware of stimuli
- Two patients showing the same blindsight behaviour, one shows activation in the V1 and the other doesn’t
31
GY absence of V1 in left hemisphere confirmed by MRI
| -Bridge et al (2008)
- MT and V5 same thing in higher areas
- (A) Normal brain scan showing activity in motion area MT in both hemispheres
- (B) GY arrow indicates location of V1 lesion (left hemisphere) – has no primary visual cortex
- Note: Activity in motion area V5/MT in both hemispheres for GY and controls
- Evidence of cortical plasticity in GY
- Diffusion-weighted MRI -Evidence of novel pathways in GY:
- From right LGN to left MT/V5
- Cortico-cortico pathway from MT/V5 both hemispheres
32
Spared regions in Visual Cortex (V1)
- Riddoch thought sparing in V1 may be the explanation (see also other later accounts Residual vision’)
- GY has no V1 as confirmed by MRI scans
- Baseleret al. (1999) J of Neuroscience
- Don’t have area V1 – do not have any sparred vision
33
If not always residual vision, then what?
- Multiple parallel visual pathways in the brain
- Cortical: Geniculostriate pathway around 90% of fibres. Retina-LGN-V1-other visual areas
- Subcortical: Retinotectal pathway around 10% of fibres. Retina-superior colliculus-pulvinar-dorsal stream
34
Role of sub cortical visual pathways in blindsight
- Superior colliculus (hindbrain) – transforms sensory input into movement output
- Functions:
- Eye-movements (saccades)
- Important for orienting attention
- Head movements
- Pointing
- Blink reflex
- Projects to dorsal visual stream via pulvinar
35
Discrimination in blindsight
- Wriskrantz (1974)
- Letters X or O presented in blind field
- DB asked to guess which stimulus presented (O or X) on each trial
- Performance well above chance (70-90%) if stimuli were large, correct
- Performance much worse with line orientation discrimination task
36
Implicit processing in blindsight – reaction times
| -Marzi et al (1986)
- Measure the effects of an unseen stimulus in the blind field on reaction times to targets in good field
- Presented flashes of light in a single target in a good field, double targets in a good field or double targets in both fields (good and blind)
- Had to move their eyes to the targets
37
SC?
-SC = Superior Colliculus
38
STP?
-STP –superior temporal polysensory area
39
FEF?
-FEF –Frontal eye field
40
MT?
-MT (=V5) Motion area
41
PUL?
-PUL = Pulvinar
42
What are the Two visual pathways?
- Milner and Goodale, 1995
- Two stream hypothesis
- Neural processing of vision
- Work from monkeys
- Two visual systems – one takes the route of the subcortical pathway through the retina to reach the posterior parietal cortex (dorsal pathway)
- Ventral stream (reaches the inferotemporal cortex) – object recognition. 95% of stimulus take this route
43
The mode of response: influences on blindsight
- GY asked to detect stimulus onset by: – blinking – pointing – verbal report
- Zihland von Cramon(1980); Marcel (1993)
- Blinking significantly better than pointing – better response
- Pointing sig. better than verbal report
- May reflect weak activity in dorsal stream that can
44
The mode of response: influence on blindsight
| -Hemianopic patient:
- Verbal responses to shapes at chance level
- Motor task, insert a card inside of a slot or pick up a card with his thumb and index finger
- Verbal – forced to make verbal choices
- Matching – required to match orientation and the size of objects
- Reaching and grasping correlated with shape and orientation
- Pereninand Rossetti (1996)
- Supports claims that sub-cortical pathway (to the superior colliculus) may be involved in blindsight responses
- Accurate eye and pointing responses may be mediated by indirect projections to superior colliculus and and/or dorsal visual pathway
- Ventral pathway may be required for awareness
45
Milner and Goodale’s account of blindsight
- Blindsight reflects visual activities performed by the dorsal visual pathway (‘where’ pathway) without awareness
- Ventral pathway (‘what’ pathway) is required for object-recognition and awareness
- Some blindsight patients are able to perceive motion (known as Type II blindsight - Weiskrantz)
46
Why is blindsight blind?
- What causes patients’ lack of awareness of the stimuli? Evidence of projections to visual cortex other than via primary visual cortex (V1)
- Patients can make accurate behavioural responses
- Integrity of V1 required for conscious perception?
47
Hierachical model
-Hierarchical models: damage to V1 disrupts the flow of information to other higher order regions , only the higher level extra striate areas are directly involved in visual awareness. Damage to the V1 simply disrupts the flow of information to these higher level areas
48
Interactive model
-Interactive models: recurrent connections between V1 and higher areas form functional circuits that support awareness. Proposes that V1 participants directly in visual awareness, forms dynamic recurrent circuits with the extra striate areas. V1 can determine what extra striate information reaches the pre frontal areas by supporting or failing to support the information represented in the extra striate areas
49
-GY may be a special case:
- Brain damage age 8 Plasticity – uses other visual pathways
- Repeated training over years may have resulted in other visual pathways developing
- 3 new cases damage to V1 and hemianopia:
- Had some awareness of motion stimuli (like GY) and could draw it despite absence of V1
- So: Primary visual cortex (V1) and back projections to it are not necessary for visual awareness
Cognitive
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