Announcements
http://www.umich.edu/~psycours/345/




Study Guide available on web by 8 PM tonight
Quiz next week for first hour of class.
Multiple choice, fills in, identifications
Bring pencils for scantrons
Last Lecture


Projections maps and the
homuculi
Organization of the Visual
System
Qu ickTime™ an d a
Ph oto - JPEG de com pre ssor
are nee ded to s ee th is p icture.
This Lecture


Organization of the Visual
System continued
Blindsight


what it is; how it ‘s studied;
what it tells us about human
visual information
processing.
What/Where pathways

Their discovery, their neural
origins, their manifestations
in humans
Sensitive areas are “magnified”
Field of View
Qu ickTim e™ an d a
oto - JPE G de com pres s or
nee ded to s e e th is pic ture .
Cortical Map of Visual Field
Receptive Field:
the region of the sensory
surface that makes a cell fire.
Cortical Magnification
• Each neuron in area 17 has a retinal receptive field
• More neurons have foveal receptive fields
Pathway from Eye to Brain
Geniculo-Striate pathway





Optic nerve carries
signals from retina.
Decussation at optic
chiasm (optic tract)
Synapse at LGN of
thalamus
Optic radiations to
occipital lobe
AREA 17; Striate Cortex
QuickTime™ and a
Photo - JPEG decompressor
are needed to see this picture.
LVF input to RH
The connections

RVF input to LH

Left Eye
 Nasal hemiretina- LVFprojects to right
hemisphere
 Temporal hemiretina- RVFprojects to left hemisphere
Right Eye
 Nasal hemiretina- RVFprojects to left hemisphere
 Temporal hemiretina- LVFprojects to right
hemisphere
nasal
To cross at optic chiasm
uncrossed
uncrossed
Vision requires cortex… or does it?
LORE of neurology until the early 70's...
LGN

Striate
extra
Striate
Reports of residual vision in animals with striate
lesions:
 Recovery after experimental field defects
 spared
light/dark discrimination
 spared localization abilities

Implication: Other structures (tectum) can
compensate for striate function.
Re-Evaluate vision in human scotomas:

Poppel, Held & Frost (1973). Residual
visual function after brain wounds
involving the central visual pathways in
man. Nature.
Task:



light flashed in scotoma
Patient looks at (saccades) to flash
location
NOTE: Patient protests: “How can
I look at something I can't see?"
Experimenter: GUESS!
Results:


Saccadic endpoint related to target
location
Text notes case D.B. (Weiskrantz)
Saccade loc
40
30
20
10
0
5
10
20
30
TARGET LOC.
Why Does Blind Sight Occur?
One theory (non-striate hypothesis):

Due to non geniculo-striate pathways


Retinotectal pathway --> direct route for saccadic eye
movement control.
Tecto-pulvinar-extrastriate --> indirect route for manual
and guessing responses.
LGN
Retinotectal
pathway
Striate
Pulvinar
S.C.
tectopulvinar pathway
extra
Striate
Alternative to Nonstriate Hypothesis:
Cortical (Striate) Islands


Fendrich, et al. (1992).
 detailed perimetry,
retinal stabilization
 revealed islands of
vision in scotoma
Implications:
 Spared tissue in Area
17 can explain residual
vision.
 Colliculus may not
mediate all blindsight
WHY is consciousness lacking?
Two possibilities

Non striate theory: primitive SC
circuitry SC is inadequate for
"awareness".
 Cortex necessary for awareness

Both theories: The weak visual signal
is below threshold for consciousness.
 non-striate theory- SC only gets
weak retinal input.
 Cortical Islands- tissue fragments
are insufficient for consciousness-NOTE: cortex does not equal
consciousness.
Lessons from Blindsight
Implicit vs Explicit (conscious) Knowledge.


Parallel operations
Yield products (representations) for different
behaviors
Human residual visual is “nonfunctional”
compared to animals.



humans "residual" capacities seen only with
experimental methods.
nonhuman species may depend more on tectum
Encephalization of visual (WHAT & WHERE)
function in primates and humans.
Announcements
http://www.umich.edu/~psycours/345/




Study Guide available on web by 8 PM tonight
Quiz next week for first hour of class.
Multiple choice, fills in, identifications
Bring pencils for scantrons
The What and
Where Pathways
The Ungerleider & Mishkin (1982) Experiment


Task 1:
Object discrimination
Task 2:
Landmark discrimination
study an object
select the familiar object*
(reward)
• select foodwell closest to
the TOWER
temporal lesions
impair OBJECT TASK
parietal lesions
impair LANDMARK TASK
Conclusion:


VENTRAL stream processes identity information
DORSAL stream processes spatial information
Logical basis for this inference:
1) Focal parietal lesion --> selective deficit,
dissociation: “where” impaired, “what” intact
2) Focal temporal lesion --> selective deficit,
dissociation: “what” impaired, “where” intact
DOUBLE DISSOCIATION
Inadequacy of a single
dissociation
Consider the following hypothetical
outcome:
 Parietal & Temporal lesions impair the
landmark task, but neither impaired
the object task
 What does this result mean?
 A) both brain areas contribute to
spatial processing?
 B) the tasks differ in difficulty?
Double Dissociation:
Experimental
strategy



2 brain areas (X,Y)
2 different tests
(T1,T2).
Result


Lesion of X
impairs T1 not T2
Lesion of Y
impairs T2 not T1
DOUBLE DISSOCIATION
TASK
PERCENT CORRECT

1
2
Locus X Locus Y
BRAIN REGION
Double Dissociation Logic Applied
PERCENT CORRECT
TASK
1
2
Locus X Locus Y
What/Where DISSOCIATION
PERCENT CORRECT
DOUBLE DISSOCIATION
TASK
Object
Spatial
Temporal Parietal
Why do these separate pathways exist?

Different functions:




NEED special purpose machinery.
have different computational
demands.
require different types of information.
How does the input to these
pathways differ?
RETURN to the Retina:
1. photoreceptors (rods and cones)
perform transduction
2. Signals sent to RETINAL GANGLION
CELLS (RG).
3. Convergence: many photoreceptors
--> one RG cell
M and P Retinal Ganglion Cells

RG Cells are not just light detectors.



Cells classified by what "turns them on"
receptive field properties of cells
M cells
a) project to Magnocellular layers of LGN
b) dominant in DORSAL/WHERE stream
c) also go to SC
d) fast conducting, colorblind, low acuity

P cells
a) project to Parvocellular layers of LGN
b) dominant in VENTRAL/WHAT stream
c) slow, color selective, high acuity



M cells --> Magnocellular pathway
P cells --> Parvocellular pathway
Their output remains segregated in V1 & beyond
Cytochrome oxidase stain reveals subregions in V1
A Schematic of What vs. Where
What vs. Where in Humans

Focal lesions produce selective color or
motion blindness.
cortical color blindness (achromatopsia)
 motion blindness (akinetopsia)
Positron Emission Tomography (PET) studies in
Humans reveal:
 Motion Area distinct from color area
 (e.g. Zeki and colleagues, 1990.)


Artwork pre and post
achromatopsia
Achromatopsia





Inability to perceive color-- color knowledge
and color naming can be intact.
acquired after cortical brain damage
distinct from congenital color blindness
(photoreceptor abnormality)
Subjective reports...
Lesion locus: bilateral occipito-temporal
lesions associated w/upper visual field
deficits.
Akinetopsia



Acquired inability to motion
Subjective reports...
Lesion locus: bilateral occipito-parietal
involving area MT/V5.
PET Activation Study Logic
• Perceptual/cognitive
activity mediated by
localized neural activity.
• Blood flow changes
accompany regional
changes in neural activity.
• Blood flow changes
measured by monitoring
distribution of radioactive
tracer.
Regions active in response to COLOR
Regions active in response to MOTION