1. Lecture 7 Visual Perception
(Dr Roger Newport)
 Hemianopia/Visual Field Cuts
 Blindsight
Akinetopsia
Achromatopsia
Agnosia
 Prosopagnosia
 Split Brain

2. Hemianopia (and other visual field cuts)
Bitemporal
Homonymous
Hemianopia
Quadrantanopia
Macular sparing

4. X Where/How What motion shapes colours objects and faces
M-ganglion cells
P-ganglion cells
Magno
LGN
Parvo V1 V2 V3 V4 MT V5 IT
cortex
Parietal
Where/How
What
motion X
shapes
colours
objects and
faces

5. Blindsight
Clinical features • loss of half of the field of vision • can detect and discriminate visual stimuli in blind field without awareness (e.g. colour, luminance, motion, orientation)
Neuropathology • striatal cortex (V1) damage
Diagnosis • forced choice reporting of ‘unseen’ stimuli

6. Blindsight - Famous Case DB
Visual field maps for the left (L) and right (R) eyes of a patient with blindsight. Patient D. B. could see almost nothing in his LVF. The only exception was in a small region in the upper left quadrant where he had unclear visual experiences. (From Weiskrantz et al., 1974)
DB: surgical removal of right striate cortex
unaware of visual stimuli in left field but above chance at :
Presence v absence of visual stimulus; Direction of visual stimulus ; Horizontal vs. Vertical

7. Blindsight - Famous Case DB
Finger-pointing performance by D.B. (From Weiskrantz et al., 1974)

8. Neuropathology • striatal cortex (V1) damage
Blindsight
Clinical features • loss of half of the field of vision • can detect and discriminate visual stimuli in blind field without awareness (e.g. colour, luminance, motion, orientation)
Neuropathology • striatal cortex (V1) damage
Diagnosis • forced choice reporting of ‘unseen’ stimuli
Theories • stray light • islands of vision • primitive visual pathways
stray light, but no blindsight at optic disc
islands of vision: Friedrich patient, but GY
primitive visual pathways - sparse, but widespread
Stray light. Some light from visual stimulus strays into areas that can see. But if stimulus displayed in natural optic disc blindspot, no blindsight shown so suggests light not straying into other visual areas.
Islands of visual cortex: Friedrich patient: found island of vision well away from macular sparing surrounded by functionally dead area that displayed blindsight whereas dead area did not. But GY shows blindsight across hemianopia. Able to track moving objects etc. Would require multiple ‘islands’ but MRI suggests this isn’t so.
Even in the absence of Vl in the monkey, visual
information can reach a large constellation of visual
‘association’ areas in the brain. Some of these paths arise
through parallel projections from the retina to the superior
colliculus, with further relays via the thalamus to the
cortex [16], or by direct projections to the pulvinar and
thence to the extrastriate cortex [l]. It is known that
intralaminar neurons in the LGN survive removal of Vl,
and project to V2, V4, V5 and TEO [ Recently,
a projection from the LGN to the inferotemporal cortex
has been demonstrated [2Zoo]. The LGN projections that
survive Vl removal are relatively sparse in density, but
are nevertheless widespread and probably encompass all
extrastriate visual areas.
Retina - SC - Th - Cortex
Retina - Pulvinar - Extrastriate cortex
Retina - LGN - V2/V4/V5/ TEO

9. X X Where/How What motion shapes colours objects and faces
M-ganglion cells
P-ganglion cells
Magno
LGN
Parvo V1 V2 V3 V4 MT V5 IT
cortex
Parietal
Where/How
What
motion X
shapes
colours
objects and
faces X

10. Akinetopsia (motion blindness)
Clinical features • inability to detect moving objects • defective smooth pursuit/reaching for moving objects
Neuropathology • bilateral damage to area MT (V5; T-O-P junction)

11. Akinetopsia (motion blindness) - Famous case LM
Case LM - akinetopsia
43 yr old. Sinus vein thrombosis
V5 damaged bilaterally - V1 spared
Could not see movement of objects but could see still objects. People would suddenly appear
Diagnosed as agoraphobic
Can see movements/reach for/catch very slow moving objects (< 10o/s)
LM could not speech read, but could tell forms of words from pictures
Contrast HJA (ventral stream damage) who could speech read, but not tell forms of words from pictures

12. Akinetopsia (motion blindness)
The consequences of inactivating areas V1 and V5 on visual motion perception
G Beckers and S Zeki Brain , 49-60
TMS study - Stimulated V1 and V5
Motion perception disrupted most with V5 stimulation up to 30ms after visual stimulation onset
V1 stimulation also partially disrupts motion perception, but later (60-70ms after VS onset).
Takes 30-50ms for signals to go from V1 to V5
Disruption of V5 causes motion blindness more than V1
Direct fast route from retina to V5 via pulvinar bypassing V1
Slower route to V5 through V1

13. X Where/How What motion shapes colours objects and faces
M-ganglion cells
P-ganglion cells
Magno
LGN
Parvo V1 V2 V3 V4 MT V5 IT
cortex
Parietal
Where/How
What
motion X
shapes
colours
objects and
faces

14. Cerebral Achromatopsia
Ishyhara plates

15. Cerebral Achromatopsia
Usually caused by bilateral damage to V4
(lingual and fusiform gyri (occipitotemporal junction))
characterized by an inability to identify or discriminate colour
Usually full field deficit but hemiachromatopsia possible if damage is unilateral
Still able to perceive form and motion - dissociation with akinetopsia and visual form agnosias
Achromatopsia is not:
due to peripheral damage (e.g. retina)
due to primary visual area damage
c) colour agnosia: disorder of colour categorization
d) colour anomia: disorder of colour naming

16. Cerebral Achromatopsia - Famous Case
The case of the colorblind painter by Oliver Sacks
Facts:
Auto accident
No clear damage (no bleeding)
No recollection of accident
Alexia for five days.
"Driving in a fog"
His studio was "..now utterly gray and void of colour. His canvases, the abstract colour paintings he was known for, were now grayish or black and white. At this point the magnitude of his loss overwhelmed him."
Over time he adapted. "I am completely divorced from colour."

17. Damasio et al., (1989b) in Heilman and Rothi (1993) 42 patients.
Which part of V4?
Damasio et al., (1989b) in Heilman and Rothi (1993)
42 patients.
achromatopsia associated with lesions below calcarine sulcus that damaged middle third of lingual gyrus, but not fusiform gyrus
Calcarine sulcus
Lingual Gyrus
Fusiform Gyrus

18. V1 V4

19. Cerebral Achromatopsia - dissociations
Wechsler’s Patient (1933) - colour and form dissociation
Anoxia from house fire - left virtually blind
incapable of recognizing objects and could not navigate surroundings
colour vision sufficiently preserved to distinguish shades of colours.
‘‘He knew at once the colours of small objects which he could
neither name nor tell the form of. He picked out colours on command’’
PB: Coma from electric shock. Blind, but can discriminate colours consciously
1. is patient’s ability to discriminate colour wavelength based or
2. are colour constancy mechanisms partly intact.
If 1, then expect the processing to be confined to areas V1/V
where there are many wavelength selective cells,
If 2. Then expect a participation of area V4 .
PB (Zeki) vs MS (Heywood and Cowey)
Awareness vs. constancy

20. Zeki et al., 1999. Colour processing in a blind patient
Age-matched Control PB
V1 only
Coma from electric shock.
Blind, but can discriminate colours consciously

21. No activation of V4 in PB suggests V4 = colour constancy
Wavelength info = V1/V2
Colour awareness - V4 or more anterior (IT)? MS
Don’t
know
Don’t
know, but same as above
Fig. 1. Color constancy. Zeki et al. (1) illuminated an array of colors with varying amounts of long, medium, and short wavelength light. Each color patch reflects
a constant proportion of the incident lights at any wavelength. (a) The green patch reflects 70% of the medium wavelength light. Normal observers report this
as green when it is presented surrounded by other colors but as white when it is presented in isolation. Patient PB would report this patch as green or white
depending on the intensity of the medium wavelength light. (b) How constancy was tested. Here the green patch is now illuminated by much more long
wavelength light. The proportions of available light reflected from each surface remain unchanged but the absolute levels of reflected intensity are greatly
changed, the long wavelengths now dominate. Normal observers still report the patch to be green when viewed in the presence of other colors. Patient PB,
however, no longer perceives the patch to be green and now reports it to be red or white, depending on the intensity of the light. All units are arbitrary.

22. The Agnosias
Bauer (1993) In Hielman and Rothi 1993
A failure of recognition that cannot be attributed to:
primary sensory defects
mental deterioration
attentional disturbances
aphasic misnaming
unfamiliarity with sensorially presented stimuli
Originally classified as having two types Lissauer (1889) :
Apperceptive and Associative

23. Associative Agnosia
can perceive, but not recognise objects
Good acuity etc
Can see global structure (full shape)
Can match to sample*
Can copy (see right)
But still cannot recognise objects
Cannot recognise own copy
Usually occurs following
left occipitotemporal damage
/anterior temporal lobe
Disconnection of areas associated with stored object knowledge
*but not nonmorphologically identical representations of the same object
(e.g. matching a line drawing with the real object).)

24. Apperceptive Agnosia
Can see
Can do obstacle avoidance etc
Good acuity etc, but
Cannot recognise objects
Cannot see global structure (full shape)
Cannot match to sample
Cannot copy
Rare. Usually occurs following gross damage to lateral parts of occipital lobes feeding ventral stream
Deficit in form perception
Copying example

25. Apperceptive Agnosia - Famous Case DF
Posting task
• Anoxia from carbon monoxide poisoning
• MRI shows damage in ventrolateral occipital region, sparing V1
• Normal colour/light discrimination etc.
• No blind spots
• Smooth pursuit ok
Cannot recognize many objects, particularly drawings or letters when presented visually
Cannot copy line drawings or pictures, but can draw from memory
Can do spatial tasks
Patient DF
Controls
Perceptual
matching
Posting

26. Other Agnosia
Alexia - left fusiform/lingual areas
Inability to form coherent lexical representations from letters
Topographagnosia or topographical agnosia - right lingual gyrus
Inability to navigate routes using familiar landmarks - deficit in familiar scene perception
Prosopagnosia - Can’t identify faces - even extremely familiar ones (even themselves!)
But can identify people by other means
And can recognise a face as being a face and
Can discriminate between faces.
Some P patients (e.g. LF - Bauer) show covert recognition
GSR picks up when when familiar vs. unfamiliar faces shown.
Recognition not lost, awareness of recognition lost.

28. Prosopagnosia - Famous case Dr. P
Sacks, The Man Who Mistook His Wife for a Hat
Dr. P. well educated musician and teacher
possible degenerative disease or large tumor
couldn't recognize faces
He recognised people on the basis of their "body music"-
their voices and the manner in which they moved
Would talk to people-shaped objects expecting a reply
Also had agnosia for objects - at times unable to tell the difference between his feet and his slippers 
Could recognise geometric objects by touch

29. Prosopagnosia
Brain region involved
George et al. (1999).
fMRI study of positive and reverse contrast faces.
Bilateral fusiform gyri response to faces
Right fusiform gyrus only when face became familiar
(Note contrast to Alexia)

30. Prosopagnosia
Is prosopagnosia special (i.e. is there a special face processing area in the brain) or just another type of agnosia?
Are faces a separate (special) class of objects or are faces just very difficult objects?
Are faces just very difficult objects
Or are they special because of our level of expertise?

31. Prosopagnosia
Prosopagnosia often co-occurs with other types of agnosia (anatomical coincidence of separate areas or are faces just objects?)
Are faces just very difficult objects?
Assal et al.(1984) patient MX
Farmer lost ability to recognise cows
Could recognise faces
Bruyer et al., (1983) patient RB
Can’t recognise faces
Less impaired at cows.
If faces just more difficult then shouldn’t have patients more impaired at other objects (i.e. cows).

32. Prosopagnosia
Are faces special objects, or are we face experts?
Activation of the middle fusiform 'face area' increases with expertise 
Gauthier et al., 1999
Sequential matching task
Inverted and upright. Expertise specific to upright

33. Prosopagnosia
Experts
Novices
Face and Greeble areas overlap
Face and Greeble areas don’t overlap
Suggests faces special due to expertise

34. IS FACE RECOGNITION NOT SO UNIQUE AFTER ALL?
Prosopagnosia
Conclusions?
IS FACE RECOGNITION NOT SO UNIQUE AFTER ALL?
Gauthier & Logothetis (2000)
COGNITIVE NEUROPSYCHOLOGY, 17 (1/2/3), 125–142
Faces are not “special”
They are the “default special”
in the primate recognition system
the face-selective area in the middle fusiform gyrus may be most appropriately described as a general substrate for subordinate-level discrimination that can be fine-tuned by experience with any object category. Gauthier et al

35. Prosopagnosia
But
Gauthier et al. 2004: Greebles not treated like faces
CW profound object agnosia. OK on faces, poor on greebles
Grill-Spector et al. 2004:
FFA is involved in detection and identification of faces, but it has little involvement in within-category identification of non-face objects (including objects of expertise e.g. birds, flowers, houses, guitars, cars etc)

36. Split Brain Patients
The Corpus Callosum
The two cerebral cortices
are interconnected by the
largest fiber system in the
brain, the corpus callosum
Human Commissurotomy
A neurosurgical treatment
for intractable epilepsy
Corpus callosum is
completely divided
Allows systematic
Investigation of hemispheric
specialization and integration

37. Split Brain Patients
Visual Recognition Studies
Picture presented in RVF (i.e. to LH)
Patient could name or reach for the object correctly with right hand
Picture presented in LVF (i.e. to RH)
Patients could not name/describe the object
Subjects could reach for the correct
object with their left hand
Split brains can perform independent incompatible motor commands
Say man
point to woman
Head-stone/sky-scraper
sprared (VP) v full (JW)

38. Left hemisphere specialised for language
Split Brain Patients
Left hemisphere specialised for language
cup
‘cup’
S can report ‘cup’
RH can select cup
LH cannot
spoon
S report nothing
LH can select spoon
(RH cannot), but S cannot say what it is
Patient NG
Springer & Deutsch (1998)

39. Split Brain Patients
Left hemisphere as an ‘interpreter’
70/30
Shovel to clean out the chicken shed (PS)
80/20
Birds and chimps 75% (optimisation)
Humans 63% (frequency matching)
Left Brain - 63%
Right Brain 75%
VP athlete ex.

40. Next Week Attention