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    1. Test 1: Next Monday COME TO THIS ROOM for the TEST Discussion sections meet in assigned class rooms GSI review session: Sunday 2-3pm—Watch ctools/email for details. Announcements

    2. More: Retinotopic Map Parallel Visual Pathways Blindsight

    3. Blindsight What it is Blindsight: Why it happens Parallel Cortical Pathways Mishkin & Ungerleider 1982 What versus where Double Dissociation

    4. Vision requires Area 17…or maybe not? Reports of residual vision in Animals with striate lesions (hamsters; monkeys): Recovery after experimental field defects (cortical ablations) spared light/dark discrimination spared localization abilities Implication: Other pathways can compensate for some geniculo-striate function. Can this also be true in humans??

    5. Poppel, Held & Frost (1973). Residual visual function after brain wounds involving the central visual pathways in man. Nature. Task: light flashed in hemianopic field Patient told ”Look at flash” Patient protests: “How can I look at something I can't see?" Experimenter: GUESS! Do cortically blind humans demonstrate residual vision?

    6. Blindsight More Confirmatory Results Weiskrantz and colleagues (1974): X vs. O discrimination in blind fields by human observers. Preserved visual behavior (residual vision) in the absence of visual experience How can this occur?

    7. The non-striate hypothesis… Retinotectal pathway --> direct route for saccadic eye movement control.

    8. Cortical (Striate) Islands Hypothesis Fendrich, et al. (1992). detailed (micro) perimetry revealed islands of vision in scotoma*

    9. The Two Blindsight Theories

    10. How do we determine which is correct? Could we use brain imaging to test predictions from the theories? Structural Functional

    11. Why is Blindsight blind? Why doesn’t “normal” awareness accompany residual vision? Non striate theory: SC circuitry is too primitive to mediate "awareness” Cortex is necessary for consciousness of percepts

    12. Why is Blindsight blind? Or Visual signal is weak, below threshold for consciousness. non-striate theory- SC only gets weak retinal input. Cortical Islands- tissue fragments are insufficient for consciousness-- NOTE: cortex does not equal consciousness.

    13. Lessons from Blindsight Some representations are unconscious. Implicit (e.g., localization) vs. explicit (experience) Different representations for different behaviors Human residual vision is less than animals Evident only with experimental methods. Nonprimate species depend more on tectum Encephalization of visual (WHAT & WHERE) function in primates and humans. Primates (Humans) depend more on cortex

    14. Blindsight What it is Blindsight: Why it happens Parallel Cortical Pathways Mishkin & Ungerleider 1982 What versus where Double Dissociation

    15. Parallel Processing in Vision Cortical versus Subcortical Within the Cortex What versus where

    16. What and where pathways What happens to visual information once it reaches primary visual cortex? What/Where first proposed by Ungerleider and Mishkin (1982) What happens to visual information once it reaches primary visual cortex? What/Where first proposed by Ungerleider and Mishkin (1982)

    17. Ungerleider & Mishkin (1982)

    18. Results

    19. Another Dissociation is needed…

    20. Ta Daaa….Double Dissociation

    21. Results Summary: 1) Parietal lesion --> selective deficit, single dissociation: “where” impaired, “what” intact 2) Temporal lesion --> selective deficit, single dissociation: “what” impaired, “where” intact Ungerleider & Mishkin (1982)

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