Lecture 3
Vision and Agnosias
Lecture Outline:
 Visual perception from the eye to the primary
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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?
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
The Eye
 Retina
1. Photoreceptors
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Rods – low levels of light
Cones – color
2. Bipolar cells
3. Ganglion cells
Cones
Form Eye to the CNS
 Each eye is divided into
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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
Form Eye to the CNS
 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
Visual Cortex – Primary Visual
Cortex
 Different names for primary
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visual cortex:
Brodmann’s area 17
V1
primary visual cortex
striate cortex (“striped” cortex)
Retinal Topography
Retinal Topography and
Cortical Blindness
• Damage of the
primary visual
cortex causes
blindness
Retinal Topography and Cortical
Blindness
 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
Disorders of Visual Pathway
Cortical Blindness and
Consciousness
 Case D.B.
 Area around the right calcarine fissure
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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
Visual Areas of the Cortex Outside
the Primary Visual Cortex
 ~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)
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
PET studies of “What” and
“Where” pathways
 Where task: did the
objects remain in the
same position?
 What task: did objects
change?
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
Imaging Visual Areas in Humans
 Semir Zeki – What part
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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)
Area V4
COLOUR
 Semir Zeki – What part
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of the brain processes
colour in the visual field
in humans?
PET scans
Experimental condition:
multicolor rectangles
Control condition?
Colour – area V4
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
Deficits in Color Perception Achromatopsia
 Congenital colorblindness
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(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?
“What” Pathway
 Early in the stream, the cells
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are responsive to simple
stimuli
Further up the stream, cells
respond to more complex
stimuli
Receptive field of 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
Deficits Following Damage to the
WHAT Pathway
 Visual agnosia – partial or total
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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
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
Deficits Following Damage to the
WHERE/HOW Pathway
 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 visualfield or –acuity deficits.
Subtypes of Visual Agnosia
 Apperceptive agnosia
 Associative agnosia
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
Associative Agnosia
 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 - Example
 Case F.R.A. – infarct of the left
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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)?
Associative Agnosias
Category Specificity
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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
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
 Patient C.K.
 Using hand
movements in
order to identify an
object
Special Category - Faces
 Prosopagnosia is 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?
One Possibility- Hierarchical Model
 If this model is
correct, what would
you expect
regarding the
dissociation
between object
and face
recognition
FACE PERCEPTION
OBJECT RECOGNITION
EARLY VISUAL
PROCESSING
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)
Perceives a face
No perception
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
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
Are Faces Really Special or Are They
Similar Examplars of the Same Category?
 McNeil and Warrington,
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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?
 Myles-Worsley,
Johnson & Simons,
1988
 Experience influences
the way items are
processed
Are Faces Really Special or Are They
Similar Examplars of the Same Category?
 Bornstein, 1963
 Following brain damage, avid bird watcher could
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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
Neural Mechanisms for Face
Perception
 Martha Farah (1990) –
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looked at 71
prosopagnosic patients
Bilateral lesions – 65%
29% right hemisphere
lesions
6% left hemisphere
lesions lesions
Conclusions?
Neural Mechanisms for Face
Perception
 Single-cell
recordings in
monkeys
 Various stimuli
presented
including monkey
and human faces
 Activation in the
inferior temporal
cortex
Neural Mechanisms for Face
Perception in Humans
 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
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
Neural Mechanisms for Face
Perception in Humans
Two Systems for Object Recognition?
•Alexia – reading
problems as a result of
brain damage
•Alexia left angular gyrus
•Prosopagnosia right FFA
•Alexia and
prosopagnosia rarely
occur in isolation –
involves object
recognition
Right hemisphere
Left hemisphere
• 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  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
Implicit Recognition of Faces
 In some instances
individuals with
prosopagnosia can
recognize faces
(implicitly……SCRs
and priming)