PO121 - University of Alabama at Birmingham

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Transcript PO121 - University of Alabama at Birmingham

Higher Visual Processing
2008
Timothy Gawne
Dept. Vision Sciences, School of Optometry
Worrell Bldg, Rm. 664 (Office) 235/236 (Lab)
Office Phone: 934-5495
Lab Phone: 934-2567
Email: [email protected]
So what is the visual system anyhow?
-> Optical System
-> Phototransduction (rods and cones)
-> Computation ***** Largest part by far *****
Something like 1/3 of the brain required for our full
visual capability.
The Inverse Problem!! No formal solution!!
So how does the visual system work?
-> Don’t really know! But learning fast – this lecture
hardly even skims the surface.
-> One of the most fundamental and exciting problems in
modern science
-> Ultimately bears on the issue of what is the mind, and
what is consciousness.
-> But for now, robots that ‘see’ are still very much
science fiction. A video camera can RECORD an image,
but it can not understand what it means and is thus
perceptually blind…
The major targets of the retinal ganglion cells:
RETINA  LGN  CORTEX (VISION)
 Superior Colliculus (saccades)
 Suprachiasmatic Nucleus (circadian)
 Pretectum (pupillary light reflex)
 Accessory Optic System (stabilize gaze)
Only about 10% of retinal ganglion cells do not terminate in the Lateral
Geniculate Nucleus (LGN).
The Retina -> LGN -> Cortex pathway is known as the geniculostriate or
thalamocortical system, it’s responsible for conscious vision.
‘BLINDSIGHT’: preservation of very limited ability to perform
visually guided tasks after destruction of the retina to LGN to
cortex pathway, in the apparent absence of conscious
perception.
Bottom line: take out the LGN-cortical system and you are for all
practical purposes completely blind. Lesion anywhere in
retina/LGN/primary visual cortex and you get complete loss of
conscious vision in specific parts of the visual field from one or
both eyes.
Lesioning in extrastriate visual cortex can cause more subtle
defects in the ability of a person to understand what they are
looking at, but with normal visual fields and acuity.
The LGN is part of the thalamus, which itself is part
of the diencephalon.
The thalamus contains sensory relay nuclei for all
the senses: sometimes called “the gateway to the
cortex”.
Know this slide! This is basic: real clinical lesions not usually so clean,
there are a LOT of subtleties. Key point: pre- vs. post chiasmal lesions.
There might, or might not, be sparing of macular vision with lesion #5.
Chiasm crosses fibers from
left and right, no crossing
up/down.
Monocular crescent located
deep in the calcarine sulcus
Note: this is only the MOST
BASIC description of visual
fields, you will have to do a
neuro-optometry or
neurology etc. residency to
really get all the fine points
of clinical diagnosis.
Migraine Visual Aura!
Thought to be due to
spreading depression
on the surface of
primary visual cortex.
Can you guess the
visual field properties?
Parvocellular System: Originates with the midget
ganglion cells in the retina, connects to parvo cells in
LGN, is most strongly associated with extrastriate
visual areas in the inferior temporal lobe. Neurons
respond well to color and fine detail, not so strongly
to rapid motion or low contrast.
Magnocellular System: originates with the parasol
ganglion cells in the retina, connects to magno cells
in LGN, more strongly associated with extrastriate
visual areas in the posterior parietal lobe. Neurons
respond well to rapid motion and low contrasts, not
so well to color or fine detail.
1,4,6, cross the river
styx
2,3,5, stay on the
same side!
LGN relay neurons project (I.e., send axons) to cortex.
LGN relay neurons have response properties that are very
similar to the ganglion cells that contact them.
LGN interneurons make only local connections.
There are more interneurons than relay neurons!
LGN neurons get feedback connections from cortex. (The
one-way connection from retina to rest of brain is unique in
the visual system).
LGN gets other inputs as well. For example: from brainstem
and perigeniculate.
-> In primates (nearly) all visual information that gets to
cortex must first go through primary visual cortex. Four
main synonyms for this part of cortex:
-> Primary Visual Cortex
-> Area V1
-> Brodmann’s area 17
-> Striate cortex
It’s called striate cortex because of a heavy band
of myelinated axons in layer 4, the stria of Gennari,
about the only landmark you can see in cortex without
special stains.
The LGN to V1 pathway is known as the thalamocortical
or geniculostriate pathway for vision.
Points: pial surface vs. white matter border, ‘vertical’ vs.
‘horizontal’ organization, three major classes of cortical
neurons (pyramidal, spiny stellate, smooth stellate), feedback
connections.
V1 SIMPLE CELLS have receptive fields with
discrete excitatory and inhibitory subregions, but
these regions are elongated into strips. Thus,
simple cells are selective for orientation.
V1 COMPLEX CELLS have NO
discrete excitatory and inhibitory
subregions in their receptive fields.
Selective for orientation regardless of
small shifts in position or changes in
contrast (i.e., switching black and
white).
Artists have long known that lines edges and contours - are of great
importance in vision (think how
expressive a few lines in a cartoon can
be). The V1 neurons that respond to
oriented lines are presumably analyzing
an image for contours and edges, which
is likely critical for vision.
Orientationselective
neurons in V1
area arranged in
cortical columns
specialized for
analyzing a
specific
orientation,
region of space,
and eye of origin
(Ipsi or Contra).
Grossly simplified
block-diagram of
the cortical visual
system
Extrastriate visual
cortex is much
larger than striate
cortex
Many Bothans
died to give us
this information.
Even more
grossly
simplified blockdiagram of the
cortical visual
system!
Like all really
complicated
systems, never
drawn the same
way twice!
(Note Bene: The
dorsal and
parvo parts of
the LGN are not
related to this
cortical divison)
Very crudely:
DORSAL PATHWAY: “WHERE” stream of visual processing: magno.
VENTRAL PATHWAY: “WHAT” stream of visual processing: parvo.
V2
-> Closely associated with V1
-> BOTH magno and parvo sections
-> Neurons in V2 have, at first glance, roughly similar
properties to those of neurons in V1. Small receptive
fields, often selective for orientation of a visual stimulus.
Neurons in V2 seem to have receptive field properties a lot like those
in V1, but are somehow better able to infer the existence of ‘illusory’ or
hidden contours from contextual information.
V4
-> One of the larger and more important of the post-V1/V2
visual cortical areas. Identified in Rhesus monkeys, but
probably has a homolog in humans.
-> More of a ‘parvo’ sort of pathway. ‘Ventral Stream’
-> More complex responsivities to shapes than just
oriented lines (real or imagined). Larger RF size.
-> Complex color properties (used to be thought of as the
color center, now know that it does more than just color)
-> Attentional effects become easier to elicit
-> Lesions cause more subtle problems than just visual
field defects.
V4 neurons often have more complex shape selectivities. Most V1 cells
can be excited by an oriented line, but many V4 cells respond best to
spirals, curves, angles, and other things a little more complicated than just
a single line.
IT
-> Inferior temporal cortex (IT, TE, TEO, etc.)
-> Last of the hierarchy of (more-or-less) purely visual
areas in the ventral (‘parvo’, ‘what’) stream.
-> Neurons can have very large receptive fields…
-> …but specificity for visual stimuli can be VERY high
-> Lesions of IT can have devastating consequences for
the ability to recognize specific objects (e.g. faces:
PROSOPAGNOSIA) with no corresponding loss of acuity
or visual field deficits.
-> Large attentional effects
-> Lesions of temporal cortex can cause visual field
deficits by interrupting the passing fibers of Myer’s loops.
MT/V5
-> Middle Temporal cortex. MT is widely studied but is only a
small (although very important) part of the dorsal stream. MT
does motion! Cells respond well to motion, activity
correlates with perception of motion, lesions interfere with
motion perception, stimulation biases direction of perceived
motion.
Important Things to Know
• Targets of the retinal ganglion cells,
laminations of LGN, pupillary light reflex.
• Visual field defects resulting from lesions in
the retina-LGN-striate pathway
• Receptive field properties of neurons in
LGN, Striate cortex (simple + complex), and
IT cortex.
• What is V1 (+synonyms), V2, V4, IT, MT
• Never fight a land war in asia.