1. COGS 172 VISION CONTINUED More on Face Processing Dorsal System, Vision for Action
Cogs 172 – A.P. Saygin

2. Agnosia Videos
Apperceptive

3. Are faces “special”?
How to test?

4. Are faces special? How to test? How selective is the deficit?
Are there “face areas” in healthy brain? …

5. Are there patients with selective face processing impairments?
Yes, there are patients with relatively selective face processing deficits.
Bruyer et al. (1983)
Mr. W, farmer with prosopagnosia, could recognize his individual cows
McNeil & Warrington (1993)
WJ – severe prosopagnosia
Became sheep farmer and could learn to recognize sheep faces, but not human faces.
 Dissociation

6. What about the reverse? Is there a “double dissociation”?
Would mean the systems could be separable.
Assal, Faure, & Anderes (1984)
Farmer MX: “zooagnosia”
Able to recognize people, but not cows
 Double Dissociation

7. But be aware
Such selective deficits are the exception rather than the norm Most patients have other deficits

8. Are faces inherently “harder”?
Importance of comparison to general population
Farah, Klein & Levinson, 1995 (see Farah reading)
LH: Prosopagnosia since college
Normal controls: 87% faces, 67% frames
Patient LH: 64% faces, 63% frames
LH was disproportionately impaired at face recognition relative to non-face recognition relative to normal subjects

10. Face Inversion

11. Inverted faces are processed more like objects
Face Inversion
Inverted faces are processed more like objects

12. Face Inversion and Prosopagnosia
Farah’s matching task (was it the same or different?)
Controls
Upright: 94%
Inverted: 82%
Prosopagnostic patient
Upright: 58%
Inverted: 72%
Patient does not benefit from upright face advantage
Actually has an advantage for inverted faces

13. Face-selective regions in the human brain: What other evidence?
fMRI “Fusiform Face Area” (FFA) - Nancy Kanwisher and colleagues But Isabel Gauthier and colleagues showed that FFA responds to cars and birds and “greebles” in car/bird/greeble experts

14. Faces may be “special” but…
There are multiple areas important for face processing
In addition to FFA, other posterior cortical regions
Occipital face area (OFA), Superior temporal sulcus (STSFA)
Amygdala
Hippocampus, parahippocampal gyrus
Also note prosopagnostic patients can recognize that a face is a face… (Compare to object/form agnosia)

15. Vision What/Where

16. “Vision for Action” What can patients teach us?
They have taught us a lot about the dorsal and ventral streams

17. What vs. Where Initial evidence: Experiments with monkeys
What pathway lesions
Unable to discriminate objects
Where pathway lesions
Unable to locate objects

18. Perception/Action
We don’t just passively perceive or locate things (“where”). Perception guides action.
Posterior parietal neurons important for eye and hand movements to spatial locations.
But instead of monkey physiology, one of the most important lessons in this field came from brain disorders.
Especially patient DF
David Milner and Mel Goodale

19. Patient DF Anoxia from carbon monoxide poisoning
Bilateral ventrolateral occipital lesion - spares V1
No blind spots
Normal color vision, brightness discrimination
Normal smooth pursuit
Cannot recogpy line drawings or pictures but can draw from memory

20. DF: Visual Agnosia Cannot recognize objects when presented visually.
Especially hard time with drawings and letters
Cannot copy line drawings or pictures but can draw from memory
Cannot recognize objects when presented visually. Especially hard time with drawings and letters

22. Orientation Matching Task

23. Reaching and Posting Task

24. DF: Object size Cannot estimate size of objects in front of her
Can estimate size if she is to reach for the object
Precision grip formed accurately from start of reach

25. What do you think would happen if DF delayed her reach?

26. What do you think would happen if DF delayed her reach?
2 sec and 30 sec delays
At both delays, the precision grip was lost.
(Eyes closed)
Normal subjects can do well at 30 sec
Means that action must be “natural”
Normals can probably “visualize” the object and pantomime the reach - but DF has impaired ventral stream so cannot visualize.

27. Implications on awareness
Harder to “fool” the dorsal stream but you are usually not aware of it.

28. DF: Summary
Cannot “see” when asked to do a perceptual task on the same visual scene
Can “see” when asked to do an active task on the exact same scene
DF’s “vision for action” is intact -- dorsal stream
Ventral stream damaged/disconnected.

29. Can patients have other visual systems selectively damaged?

30. Cerebral Achromatopsia: “Color blindness”
Deficit of color processing caused by acquired cerebral lesions
Colors look “dirty”, “washed out”, “lights are dim”
Inability to identify or discriminate color.
Usually affects a portion of visual field but can be full visual field
How is it tested?

31. Achromatopsia
Must make sure problem is not in color naming or color categorization
Ishihara plates
Farnsworth-Munsell 100 Hue Test

32. Achromatopsia
Usually V4 damage - anatomically lingual gyrus, fusiform gyrus, or white matter between the regions
Lingual gyrus seems more strongly implicated than fusiform gyrus
Form and motion perception is usually intact
Concurrent alexia and object agnosia is fairly common
Color knowledge is intact (they can answer semantic questions)
But color imagery is often also affected

33. Cerebral Akinetopsia: “Motion blindness”
Deficit of motion processing caused by acquired cerebral lesions
Because motion cues serve many purposes, a range of deficits can result
E.g., Difficulty using motion to find objects
Pursuit eye movements are often impaired

34. Motion blindness
Patient MP: “When I’m looking at the car first, it seems far away. But then when I want to cross the road, suddenly the car is very near.”
Strobe-like, static images
Usually
Good static visual acuity
Perception of tactile and acoustic motion intact
Accurate localization of visual targets by saccadic eye movements
Relative preservation of face and object recognition, reading, and color vision

35. “Patient LM: The patient had great difficulty pouring coffee into a cup. She could clearly see the cup's shape, color, and position on the table, she told her doctor. She was able to pour the coffee from the pot. But the column of fluid flowing from the spout appeared frozen, like a waterfall turned to ice. She could not see its motion. So the coffee would rise in the cup and spill over the sides.
More dangerous problems arose when she went outdoors. She could not cross a street, for instance, because the motion of cars was invisible to her: a car was up the street and then upon her, without ever seeming to occupy the intervening space.”
Was diagnosed with agoraphobia…
Lesions: Bilateral dorsolateral visual association cortex, spares area V1, covers V5/MT.
Could see/catch very slowly moving objects.

36. Motion Blindness: Lesion Sites
Bilateral MT/V5 lesions
Human monkey motion area analogies - not completely clear
Temporoparietal, near angular gyrus
Parieto-occipital
As part of another disease
(Balint's syndrome or Alzheimer's disease)
Deficits of motion perception (not as severe) can also occur with lesions in parietal insula and midline cerebellum
Transient cases of motion blindness have been reported as side effects of antidepressant medication (SSRI)