Vision and agnosias

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1. Vision and Agnosias
تخانش و یرادید کاردا یصصخت هاگراک
هدازیلع یدهم رتکد
ناتسبات1396

2. Lecture Outline:
Visual perception from the eye to the primary
visual cortex (pp. 23-28)
Vision beyond primary visual cortex: analyses of
movement and colour
Higher perceptual abilities: recognition of objects
and disorders of visual recognition –agnosias
Are faces special objects?
Are there two ways of processing visual
information?

3. Vision
Vision is important for primates
~50% of cortex devoted to visual perception
Stimulus in the visual system is light (electromagnetic
energy)
We only see a small band of electromagnetic waves

4. The Eye
Retina
1.Photoreceptors
Rods –low levels of light
Cones –color
2.Bipolar cells
3.Ganglion cells

5. Cones

6. Form Eye to the CNS
Each eye is divided into
two identical halves
Within each eye, one half
received stimulation from
the left visual field and
the other from the right
visual field
Optic nerve
Lateral or temporal
branch stays on the same
side
Medial or nasal branch
crosses over
Optic chiasm

7. Lateral geniculate nucleus
(LGN) of the thalamus
Primary visual cortex
(90%)
Geniculostriate pathway
Superior colliculus (10% -
projects back to thalamus
and then to cortex) –
tectopulvinar pathway
Form Eye to the CNS

8. Form Eye to the CNS

9. Different names for primary
visual cortex:
Brodmann’s area 17
V1
primary visual cortex
striate cortex (“striped” cortex)
Visual Cortex –Primary Visual
Cortex

10. Retinal Topography

11. Retinal Topography and
Cortical Blindness
•Damage of the
primary visual
cortex causes
blindness

12. Hemianopia–loss of
pattern vision in either
the left or right visual
field
Quadrantanopia–
blindness in one
quadrant of the visual
field –damage to the
optic tract, LGN or V1
Retinal Topography and Cortical
Blindness

13. Disorders of Visual Pathway

14. Case D.B.
Area around the right calcarine fissure
was removed for treatment of angioma
Reported not seeing anything in the left
visual field
Able of pointing out where the light was
in the left visual field
Blindsight–residual visual abilities
within a field defect in the absence of
acknowledged awareness
Importance of subcortical visual
pathways
Cortical Blindness and
Consciousness

15. ~30 cortical visual
areas with distinct
functions
Each visual area has
a topographic
representation of
external space in the
contralateral
hemifield (however,
these get ‘less’
topographic as we
get further up in the
system)
Visual Areas of the Cortex Outside
the Primary Visual Cortex

16. Two General Projections From the
Primary Visual Cortex
Dorsal stream –Occipito-parietal stream spatial
perception –action-“where” or “how to”
Ventral stream –Occipito-temporal stream object
perception –identification –“what” stream

17. PET studies of “What” and
“Where” pathways
Where task: did the
objects remain in the
same position?
What task: did objects
change?

18. Area MT or V5
MOTION
Cells in area MT
respond to movement
but not color
For example, this
particular neuron in this
monkey’s V5 area
responds best when
stimulus moved down
and to the left

19. Semir Zeki –What part
of the brain processes
movement in the visual
field in humans?
PET scans
Experimental condition:
black-and-white collage
set in motion
Control condition?
Motion –area V5 (MT)
Imaging Visual Areas in Humans

20. Area V4
COLOUR
Semir Zeki –What part
of the brain processes
colour in the visual field
in humans?
PET scans
Experimental condition:
multicolor rectangles
Control condition?
Colour –area V4

21. Deficits in Motion Perception:
Akinetopsia
Case M.P.
Bilateral damage to
teporolateral corticies (MT?).
“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.”
Color discrimination OK
Object recognition OK

22. Deficits in Color Perception -
Achromatopsia
Congenital colorblindness
(dichromats) vs. acquired
colorblindness
Usually associated with damage to V4
Colorblind painter –case J.I.
Object recognition OK
Improved acuity
People were “rat-colored”
Dreams?

24. “What” Pathway
Early in the stream, the cells
are responsive to simple
stimuli
Further up the stream, cells
respond to more complex
stimuli
Receptive fieldof a cell is the
area of visual space to which
the cell is sensitive
Cells in the primary visual
cortex have small receptive
fields
Cells further down the “What”
stream have large receptive
fields

26. Deficits Following Damage to the
WHAT Pathway
Visual agnosia–partial or total
inability to recognize visual stimuli,
unexplainable by a defect in
elementary sensation or reduced
level of alertness or memory
NO GENERAL LOSS OF
KNOWLEDGE
Different from other neurological
conditions such as Alzheimer’s
disease
Tactile agnosia (Asterognosis)
Auditory agnosia

27. Dissociating Deficits in WHAT and
WHAT/HOW Pathways
Patient D.F. severe disorder of
object recognition following carbon
monoxide poisoning that produced
damage in the lateral occipital
cortex
Dissociating the “what” and
“where” system
D.F. had no problem with the
“where” pathway

28. Patient V.K. –bilateral
hemorrhages in the
occipitoparietal regions
Deficits with “how/where”
stream but not “what”
stream (can recognize
objects
Optic ataxia–difficulty in
using visual information to
guide actions that cannot
be ascribed to motor,
somatosensory, or visual-
field or –acuity deficits.
Deficits Following Damage to the
WHERE/HOW Pathway

29. Subtypes of Visual Agnosia
Apperceptive agnosia
Associative agnosia

30. Apperceptive Agnosia
Apperceptive agnosia–is a
fundamental difficulty in forming
percept (a mental impression of
something perceived by the
senses)
cannot recognize, copy, or match
objects, however elementary
sensory functions appear relatively
intact (i.e., patients are not blind).
usually bilateral damage to lateral
portions of the occipital lobes
(what stream–early deficits in
visual perception)
Often associated with carbon
monoxide poisoning

31. Associative agnosia–basic visual
information can be integrated to forma
meaningful perceptual whole, yet that
particular perceptual whole cannot be
linked to stored knowledge
What is affected? “higher cognitive”
level of processing that is associated
with stored information about objects –
that is with memory.
Patients have either lost access to
memories of what things should look
like or actually lost these memories
Damage to regions in ventral stream
that are further up the processing
hierarchy, such as the anterior temporal
lobe
Associative Agnosia

33. Associative Agnosia -Example
Case F.R.A. –infarct of the left
posterior cerebral artery
Copying of objects OK
Can describe objects when they
are named
Can segment a complex drawing
into parts (apperceptive patients
cannot do this)
He could not name these objects
How would test if this is a
language problem (finding words
for objects)?

34. Patient J.B.R.
Herpes simplex encephalitis
Living objects (6% correct)
Inanimate objects (90% correct)
Other patients the other way
around
Why is this the case?
Associative agnosia loss of
semantic knowledge
Semantic knowledge has
categories
Associative Agnosias
Category Specificity

35. Why Is It More Likely That Animals
Won’t be Recognized?
Manufactured objects are
manipulated
Associated with kinesthetic and
motoric representations
Manufactured objects are
easier to recognize because
they activate additional forms of
representations
Individuals can “where” or “how
to” pathway to derive
knowledge of an object might
be

36. Patient C.K.
Using hand
movements in
order to identify an
object

37. Special Category -Faces
Prosopagnosiais the inability to visually recognize familiar
faces including their own
Can recognize people by their voice or birthmark or
characteristic hairdo.
Prosopagnosia patients can be object-agnosia free
Are faces special?
Do the processes for faces and object involve physically
distinct mechanism?
Are the systems (object and face recognition) functionally
independent?
Double dissociation?
Do the two systems process information differently?

38. One Possibility-Hierarchical Model
If this model is
correct, what would
you expect
regarding the
dissociation
between object
and face
recognition
EARLY VISUAL
PROCESSING
OBJECT RECOGNITION
FACE PERCEPTION

39. Dissociations of Face and Object
Perception
Patient C.K. was
presented with
Giuseppe Arcimbaldo’s
paintings
severe object agnosia
but no prosopagnosia
Hierarchical model
probably not correct
2 parallel system
(object recognition and
face recognition)
No perceptionPerceives a face

40. More Evidence that Faces are
Processed Separately
Yin, 1970
It is more difficult to
process inverted
faces
When inverted,
faces are processed
as objects
It is less difficult to
recognize inverted
objects

42. More Evidence that Faces
are Processed Separately
Tanaka & Farah 1993
Face perception not simply analysis
of parts
For house perception it did not
matter if the house was presented
as a whole or in parts
Faces need to be perceived as
whole

43. McNeil and Warrington,
1993
Farmer with
prosopagnosia
Tested on human faces –
failed
Tested on sheep faces –
OK
Is prosopagnosia due to
the fact that faces are
similar members of the
same category?
Are Faces Really Special or Are They
Similar Examplars of the Same Category?

44. Are Faces Really Special or Are They
Similar Examplars of the Same Category?
Myles-Worsley,
Johnson & Simons,
1988
Experience influences
the way items are
processed

45. Are Faces Really Special or Are They
Similar Examplarsof the Same Category?
Bornstein, 1963
Following brain damage, avid bird watcher could
no longer distinguish between different bird
species
Sergent & Signoret, 1992
Toy car expert (5000 in his collection)
Following brain damage he became
prosopagnosic
He was able to identify different cars

46. Martha Farah (1990) –
looked at 71
prosopagnosic patients
Bilateral lesions –65%
29% right hemisphere
lesions
6% left hemisphere
lesions lesions
Conclusions?
Neural Mechanisms for Face
Perception

47. Neural Mechanisms for Face
Perception
Single-cell
recordings in
monkeys
Various stimuli
presented
including monkey
and human faces
Activation in the
inferior temporal
cortex

48. Human fMRI studies
Face stimuli
associated with
activation of the right
fusiform gyrus
Fusiform face area –
FFA
FFA is also activated by
other stimuli
Car and bird
experts
Neural Mechanisms for Face
Perception in Humans

49. Activation of the FFA by Non-Facial
Stimuli
Individuals were
trained to be
experts at
recognizing
“greebles”
In “greebles”
experts, FFA is
activated during
identification

50. Neural Mechanisms for Face Perception in
Humans

51. Two Systems for Object Recognition?
•Alexia–reading
problems as a result of
brain damage
•Alexia leftangular gyrus
•Prosopagnosia rightFFA
•Alexia and
prosopagnosia rarely
occur in isolation –
involves object
recognition
•High incidence of alexia and agnosia
•High incidence of prosopagnosia and
agnosia
•No patient with prosopagnosia and alexia
without agnosia
•Object recognition by two routes
Right hemisphere Left hemisphere

52. Right Hemisphere Holistic
Left Hemisphere Analytic
Extreme cases
Patients with either left-or right
sided strokes were presented
with stimuli and later asked to
recall this stimuli
Patients with left-sided lesions
show intact global features but
no detail
Patients with right-sided lesions
produce detail only

53. Implicit Recognition of Faces
In some instances
individuals with
prosopagnosia can
recognize faces
(implicitly……SCRs
and priming)