Blindsight Flashcards

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1
Q

What is cortical blindness?

A

Damage to the cortex rather than damage to the eyes

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2
Q

How did blindsight research start?

A

Lesion-induced blindness in monkeys (Brwon and Schaffer 1888) and cortical retinotopy after the introduction of the high-velocity bullet which made discovery of cortical retinotopy possible due to the small wounds (no imaging techniques)

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3
Q

What are different types of visual field defects?

A

Hemianopia, quadrantanopia and scotoma

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4
Q

Is cortical blindness always blind?

A

Early debate. Munk and Shaffer said that vision patially returns (monkeys), while Holmes argued that occipital lesions completely obliterated vision, and Poppelreuter argue that occipital lesions never rendered a patient absolutely blind

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5
Q

What is the Riddoch phenomenon?

A

Reported that patients with occipital lesions, while blind to stationary stimuli, reported some visual experience when objects in blind field moved vigorously

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6
Q

How have monkey studies supported Riddoch?

A

Hymphrey observed Helen who had a removed (bilateral) striate cortex yet could avoid obstacles, grasp objects and catch a flying fly

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7
Q

What is the Brodmann number for the primary visual cortex?

A

Area 17

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8
Q

What is blindsight?

A

The ability of patients with damage to their primary visual cortex to detect, discriminate and localise visual stimuli presented in areas of their visual field in which they report they are subjectively blind (dissociation between awareness of visual stimuli and the ability to respond appropriately)

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9
Q

What study shows the first report of blindsight?

A

Poppel, Held and Frost 1973. Wanted to see if patients with visual scotomata as a result of damage to visual cortex could move their eyes to gaze at spots of light presented in blind regions. They could (a bit). Not perfect but not random

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10
Q

What types of experimental design are typically used in blindsight?

A

Patients reluctant to perform ‘free-response’ procedures so applied ‘forced-choice’ is used (Wiskrantz et al 1974). Forced choice with commentary can also be useful

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11
Q

What is the case study of DB?

A

Migraines caused by enlarged blood vessels in right visual cortex. Area removed, including much of the striate cortex (right hemisphere). Became phenomenally blind in left field (left hemianopia). Was able to move eyes towards light flashed in scotoma and point to light but denied seeing it (much better than chance)

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12
Q

What areas are involved in geniculate projections to V1?

A

Retina, optic nerve, lateral geniculate nucleus, optic radiation and striate cortex

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13
Q

What areas are involved in the non-geniculate projections to V1?

A

Superior colliculus and pulvinar. Suggest of pathway explains preserved visual abilities in those with blindsight as it bypasses v1

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14
Q

What is subcortical mediation?

A

Subcortical systems mediate many of the body’s responses to light. Projections from retina to colliculus can mediate reflexive eye-movements without cortex

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15
Q

What does blindsight, for motion, rely on?

A

Direct pathways from LGN to V5/MT+. Changes in connectivity after visual cortical brain damage underlie altered visual function (Bridge et al 2008). GY, similar to controls had the route that bypasses v1 but also had a contralateral pathway from right LGN to left MT+/v5 and a substantial cortico-cortical connection between MT+/V5 bilaterally

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16
Q

What do Ajina and Bridge 2019 argue about blindsight and the pulvinar?

A

Blindsight relies on a functional connection between hMT+ and the lateral geniculate nucleus, not the pulvinar

17
Q

What are the alternative explanations of preserved visual abilities in blindsight?

A

Light scatter, islands of spared cortex, degraded normal vision

18
Q

What are uncontroversial findings of spared functions in blindsight?

A

Detection and location of luminance transients and contrast transients

19
Q

What are controversial findings of spared functions in blindsight?

A

Motion. GY can detect motion but cannot discriminate motion direction. Appears to be responding to onsets and offsets at fixed locations rather than the motion signals we normally use

20
Q

What are partly uncontroversial findings of spared functions in blindsight?

A

Colour discrimination. Boyet et al 2005 TMS induced blindsight in normal participants led to successful colour and orientation discrimination, though it is very difficult to rule out artefacts

21
Q

What are some maybe uncontroversial findings of spared functions in blindsight?

A

Limited form processing. Perhaps just line or grating orientation (discrimination problems)

22
Q

Is there blindsight for facial expressions?

A

De Gelder et al 1999: 4 movies with either happy, sad, angry or fearful facial expressions. Recognition above chance for most conditions and significantly above chance for dynamic vs static stimuli

23
Q

Why is the research on facial expressions controversial?

A

Because it is a simple system but complex information that is being transmitted

24
Q

What did research with GY on facial expressions show?

A

Faces presented to blind hemifield did not evoke increased response in visual cortex. Response to unseen fear in amygdala (response related to pulvinar and SC response, suggestive of pulvinar pathway)

25
Q

How blind is blindsight?

A

Commentary responses are not always negative (some patients do report awareness of stimulus). Subjects sometimes experience something (but is it seeing?). Temporal frequency influences awareness (faster shows more awareness in commentary) similar to Riddoch phenomenon

26
Q

What did He, Cavanagh and Intrilligator 1996 find?

A

Used crowding task to assess role of visual cortex in awareness. Crowding eliminates ability to consciously discriminate orientation of target patch , even with unlimited viewing time at full contrast. Demonstrates an effect of orientation in absence of awareness of that orientation. These orientation-adaption effects are mediated by cells in V1. Activity in primary visual cortex does not correlate with consciousness