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Flashcards in Blindsight Deck (49)
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Who was patient TN?

-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)


What is blindsight?

-"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


How can you test blindsight?

-Stimulus moving either horizontally or vertically
-Cannot see the stimulus itself, e.g. colour, shape


What is blindsight and hindsight?

-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


What is in the hindbrain?

-Reticular formation


What did Weiskrantz – The Ferrier Lecture 1989 -Proceedings of Royal Society (1990) lead to what we know now about visual functions?

-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


What is the main pathway from the eye to the visual cortex?

-Anterior (before) and Posterior pathways (after)
-Sensory inputs -Primary visual cortex (V1) and striate cortex
-Extrastriate areas consist of V2, V3, V4,V5


Functions of visual cortex: Species differences

-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


Monkeys without primary visual cortex can:

-discriminate shapes
-maintain (reduced) acuity
-fixate and reach towards small and brief visual events
-detect movement
-Humans typically function blind


What is -Cortical blindness ?

Loss of vision following damage to visual cortex (e.g. area V1, not the retina or optic tract)


What is -Hemianopia ?

Loss of vision in one half of visual field following unilateral brain damage


How does information flow from retina to cortex?

-Information comes in through the eye and travels to Primary visual cortex via the lateral gen
-Goes to higher areas for visual processing


‘What’ and ‘where’ visual pathways (Mishkin & Ungerleider, 1982)

-‘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


Measures of blindsight?

-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


The first experimental demonstration of blindsight in humans was?

-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?”


Who was patient DB?

-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


What experiment was conducted on patient DB?

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


How did DB perform in the experiment?

-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


How did DB react to his performance?

-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


Who was patient GD?

-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...)


Further demonstration in 2 out of 4 cases?

-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


What did Rafal et al (1990) do showing lights and hemifields?

-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


Implicit measures: Galvanic skin response (GSR)

-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


Implicit measures: Pupil response?

-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


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


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


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


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


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)


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