1. Vision and Visual System Disorders
Cogs 172 – A.P. Saygin

2. Seeing is constructing

3. How vision works: The retina
Photons hit the photoreceptors. Rods, cones. Different adaption to light. Cones are mostly responsible for high acuity and color vision.
Synapse onto retinal ganglion cells. Retinal input leaves the eye via the optic nerve

4. From the eyes to the CNS
We know sensory systems “cross”, e.g. left hand is represented in right hemisphere
So the neural input from the left eye goes to the right hemisphere

5. WRONG! From the eyes to the CNS
We know sensory systems “cross”, e.g. left hand is represented in right hemisphere
So the neural input from the left eye goes to the right hemisphere
WRONG!
(although if you’re remembering something about information from the two eyes remaining segregated from your neuroscience classes that’s true)

6. LEFT VISUAL FIELD TO RIGHT HEMISPHERE AND VICE VERSA

7. Optic nerve, optic chiasm: Lateral/temporal branch stays on the same side. Medial/nasal branch crosses over.
Lateral geniculate nucleus (LGN)
Primary visual cortex
First cortical area: V1
V2, V3, …
(SC and pulvinar - important for visual function, attention and eye movements)

8. LGN Segregation by eye Segregation by function:
M CELLS in retina to MAGNOCELLULAR layers (1,2) - low res.
P CELLS in retina to PARVOCELLULAR layers (3,..6) - hi res.

9. Some areas have known functions
V4 is color-sensitive
MT and surrounding areas: Motion-sensitive

10. Retinotopy
Information travels from retina to LGN and LGN to cortex in a systematic way
Visual space is mapped onto cortical surface
Fovea is mapped larger than periphery: Cortical magnification

11. So retina is mapped onto V1 with a bit of stretching and then we see
So retina is mapped onto V1 with a bit of stretching and then we see! No, many more visual areas…
Why so many visual areas?
Some specialization, e.g. color, motion
Rarely patients will have damage to these areas and will show paradoxical deficits which help us to understand vision.
But also a lot of unknowns, a lot of redundancy.
E.g., a whole lot of retinotopy

12. The ventral stream or the WHAT pathway
The dorsal stream or the WHERE pathway
M: poor spatial resolution, good temporal resolution
P: good spatial resolution, poor temporal resolution
M cells, Magnocellular layer of LGN, V1 (upper subdivision of layer 4), V2 (thick stripes), MT, parietal lobe (“where”)
P cells, Parvocellular layer of LGN, V1(lower subdivision of layer 4), V2 (thin and interstripes), V4, inferotemporal lobes (“what”)

13. What happens if you have damage to the pathways from the eye to cortex?

18. Meyer’s loop: Through the temporal lobe
Meyer’s loop: Through the temporal lobe. Upper visual field ~ Lower part of the retina. (Since retina inverts up/down).
Note image below makes Meyer’s Loop seem more superior but in fact (like image on left) it’s more ventral and lateral.

21. Visual cortex receives blood from the PCA and also a little from MCA
Visual cortex receives blood from the PCA and also a little from MCA. This explains why macular sparing can occur even after severe occipital lobe strokes (PCA occlusion).

22. How do we test visual field?
Perimetry
Video
What do you think?

23. What happens with cortical lesions?
Hemianopia, quadrantopia
Scotoma: Blind spot in the visual field

24. Why might you not notice a small scotoma? Eye movements Filling-in

25. Why might you not notice a small scotoma? Eye movements Filling-in

26. Vision Not always “veridical” Context-dependent
Perceptual filling-in: information that is not in the sensory input. May spread from sensory input from a different part of the visual field.
Filling in is an active visual process that occurs at multiple levels of visual processing

27. We all have blind spots, but we don’t feel like we do…
Area on retina where there are no photoreceptors (behind the optic nerve). When you look with one eye, you can discover your blind spot
Experiment with your blind spot:

28. “Blindsight”

29. Blindsight: A controversy
Patient D.B.
Lesion to V1
Reported not seeing anything in the left visual field
Could point to lights in LVF!
Could “guess” X vs. O
But still said “I don’t see it” and was not consciously aware of “doing” it, and “getting it right”

30. How?
May be mediated by the subcortical pathway (especially the superior colliculus/pulvinar to MT/V5 or the “tectal pathway”)
Implications for consciousness.
Can we tell from blindsight patients, where visual awareness is located in the brain?
Readings: Quickguide (required). Cowey, 2010 review (optional)

31. Something else that can happen in vision loss: Hallucinations
Hallucinations !! But patients know they are not real.
Animals, faces, objects
Swirls, dots
Motion patterns
Still “cartoons”
What is happening? (Reading: ffytche, 2009)

32. Visual system is not simply a hierarchical bottom-up system
A lot of crosstalk. There are lateral (horizontal) connections as well as feedback connections
How our visual world is “constructed” by this system is still under study

33. Sight-recovery Long term effects of early visual deprivation
Patient MM (Fine et al, 2003, Nature Neuroscience)
Blindness ~3 years of age
Sight recovery ~43 years of age
- Reduced acuity
- Simple form, color and motion processing normal.
- Complex form, 3D form, object and face recognition severely impaired.
- Not much improvement after several years.
- Motion processing robust to deprivation
- Fine acuity and complex form and object processing require input beyond 3 years of age

34. Enhanced sensory processing in blindness
Blind individuals often have heightened sensitivity in other modalities
Can humans use echolocation? Bats, dolphins, barn owls…
See: and
Lab studies show he has limited but notable echolocation abilities. Unfortunately, patient passed away in 2009.
Most useful in context, and in learned environments.
Attention seems necessary (Roder et al., 1999, Nature)

35. V3/VP

36. From here: Thursday

37. Visual form agnosia

38. Visual form agnosia
PRESERVED acuity, brightness discrimination, color vision, & other elementary visual capabilities. Sometimes preserved shape from motion.
SEVERELY IMPAIRED form perception (pictures, letters, simple shapes, objects)
They do not have memory problems or dementia, they have knowledge of the objects.
How to test?

39. Visual form agnosia
PRESERVED acuity, brightness discrimination, color vision, & other elementary visual capabilities. Sometimes preserved shape from motion.
SEVERELY IMPAIRED form perception (pictures, letters, simple shapes, objects)
They do not have memory problems or dementia, they have knowledge of the objects.
How to test?

40. Videos

41. Videos
I’m not very sure. Guess in a minute? You got me… (when she touches) … Of course, I know what this is already, it’s a clothespin.
You won’t let me touch it? Gosh - It could be so darn many things… I don’t think I could guess that… (immediately after touching)… Lord, it’s a piece of soap.
That’s a … (seems to know it but slow to name). A pin, a safety pin.
You got me. (touches it) It’s a piece of soap. (smells it). Oh it’s a candle.

42. Apperceptive Associative
Visual Agnosia
Apperceptive Associative

43. The “copy” test
Apperceptive agnosia is mainly characterized by failures in object recognition linked to problems in perceptual processing
Patients cannot recognize, copy, or match objects.
 Mr S. Benson & Greenberg 1969

44. Apperceptive Associative

45. Associative Agnosia Trouble recognizing objects visually
Can copy -- perception seems preserved!
“Higher level”
Matching objects to stored object representations - Where is the deficit: Mnemonic or perceptual?
Perceptually similar errors
Copying is piecemeal, slow
 Rubins & Benson 1971

47. How do agnosic patients get by?
Touching
Color
Some can see motion
Form from motion?
Piece together multiple cues… General reasoning

48. Lesion tendencies Apperceptive: Occipito-temporal
Sometimes inferior parietal
Associative:
Occipitotemporal

49. Agnosia Much variability among patients
The idea of loss of global or “gestalt” perception
“Integrative agnosia” -- sometimes patients guess based on a feature or part but cannot bind into a whole; brief presentation not enough
Role of tracing, motion

50. Special subclasses of objects: Faces and words
Prosopagnosia: Impairment in the recognition of faces. Often accompanied by other impairments (e.g., place or object recognition, facial expression of emotion). Can be restricted. Use voice, hair, body movements etc.
Alexia: Unable to read. Patients with “alexia without agraphia” will be able to write but not read.
Are these distinct “modules”? Are they correlated? Can agnosic patients tell us anything?

51. Powerful deductive tools in brain disorders
Associations
Dissociations
Double dissociations
Important
- clinically
- in understanding the brain

52. Associations Behavior A and Behavior B are affected together
Suggests a relationship
There may be separate areas, damaged because they are close together
What can help?

53. Associations Behavior A and Behavior B are affected together
Suggests a relationship
There may be separate areas, damaged because they are close together
What can help? B A

54. Dissociations Behavior A impaired, Behavior B spared
So they are independent.
But maybe one task is easier
Patients fail at hard task
Spared regions of brain carry out easy task A B

55. Double dissociations
Behavior A impaired - Behavior B spared in one patient/group
Behavior B impaired - Behavior A spared in one patient/group
Independent resources
A DD between two tasks does not necessarily imply a DD between cognitive processes (Shallice, 1988)
E.g. “lesioned” neural network models with no obvious modular structure can produce data that looks like a DD (Plaut, 1995). A B

56. Major types of agnosia and lesion locations
Face
Object
Printed Word
Face, or face and object -- mostly bilateral, sometimes right
Word, or word and object – usually left
Maximum overlap in left inferior medial temporal (including parahippocampal, fusiform, and lingual gyri)

57. A little more about faces…

58. Some face processing tests
Famous faces test
Facial expressions (many patients can do)
Matching tests
Match face to different viewpoint
Match face to one you just saw (correct vs. incorrect)
Memory tests (recall, recognize)
Custom tests/experiments

59. Where are the lesions that cause prosopagnosia?
Fusiform and lingual gyri are often implicated. Bilateral, if unilateral often Right

60. But… sometimes there is no lesion
Congenital or Developmental prosopagnosia
Face recognition impairments with no known lesion or clear neurological cause
Intact “fusiform face area” and ventral visual regions - in fact intact brain
Are they just the people who are really really bad at face recognition? Or is this really a disorder?

61. Are faces special?
How would you test?

62. Are faces special? How would you test?
Is the deficit really selective?
Are there “face areas” in normals? …

64. Are there really patients with selective face impairments?
Yes, there are patients with relatively selective face processing deficits.
Bruyer et al. (1983): Impaired perception of faces but not cows.
McNeil & Warrnington, 1993: Sheep farmer - could learn to recognize sheep faces but not human faces.
---> this is a dissociation

65. What about the reverse? This would mean a “double dissociation”
Would mean the systems could be separable.
This has been reported: Assal, Faure, & Anderes (1984): Zooagnostic farmer MX
Could recognize people but not cows
---> this is a double dissociation

66. But be aware…
Selective deficits are the exception rather than the norm
Most patients will have other deficits

67. Are faces inherently “harder”?
Farah tried to find objects as ‘difficult’ as faces.
College students 87% faces, 67% frames
Patient 64% faces, 63% frames

69. Inverted faces are processed more like objects

70. Face inversion and prosopagnosia
Farah’s matching task (was it the same or different?)
Normal controls
Upright: 94%
Inverted: 82%
Prosopagnostic patient
Upright: 58%
Inverted: 72%
Perhaps evidence for a specialized face system.

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

72. Faces may be “special” but…
There are many other areas important for face processing
Occipital face area, Superior temporal sulcus (OFA, STSFA)
Amygdala
Hippocampus, parahippocampal gyrus
Also note prosopagnosics can recognize that a face is a face… (Compare to object/form agnosia)

73. Vision: What/Where

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

75. What vs. Where Initial evidence: Monkey experiments
What pathway lesions
Unable to discriminate objects
Where pathway lesions
Unable to locate objects

76. A perception/action distinction
You don’t just locate things, you do things to them - 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

77. DF Anoxia from carbon monoxide poisoning
Bilateral ventrolateral occipital lesion - spares V1
No blind spots
Normal color vision, brightness discrimination
Normal smooth pursuit
Cannot recognize objects when presented visually. Especially hard time with drawings and letters
Cannot copy line drawings or pictures but can draw from memory

78. 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

80. Orientation matching

81. Reaching and posting

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

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

84. 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.

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

86. 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.

87. Can patients have other visual systems selectively damaged?

88. 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?

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

90. 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

91. 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

92. 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

93. “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.

94. 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)