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

Agnosia Videos Apperceptive

Are faces “special”? How to test?

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

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

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

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

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

Face Inversion

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

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

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

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)

Vision What/Where

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

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

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

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

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

Orientation Matching Task

Reaching and Posting Task

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

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

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.

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

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.

Can patients have other visual systems selectively damaged?

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?

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

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

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

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

“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.

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)