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thin stripes
color perception
thick stripes
form information
pale stripes
motion perceptiion
v1
receives largest input from lateral geniculate nucleus of the thalamus and projecting to all other occipital regions; necessary to process and interpret visual information
v2
secondary processing location; has 3 distinct parallel pathways emerge from it
dorsal stream
parietal pathway; visual guidance of movement
ventral stream
temporal pathway; object and motion perception
STS stream
object and motion perception
v3
processes dynamic form, or the shapes of object in motion
v4
predominantely processes color info
v5
MT (middle temporal); involved in motion procession
damage to v4
only see in shades of gray and loss of color cognition
damage to v5
erases ability to preceive objects in motion; objects vanish when they move
damage to v3
affect for perception
damage to v1
patients report being blind, but smaller projectitons from subcortical areas to high visual areas providee some limited visioin
lateral occipital (LO)
object analysis
fusiform face area (FFA)
face analysis
extrastriate body area (EBA)
body analysis
fusiform body area (FBA)
body analysis
superior temporal sulcus (STS)
analysis of biological motion
superior temporal sulcus posterior (STSp)
moving body analysis
parahippocampal place area (PPA)
analysis of landmarks
lateral intraparietal sulcus (LIP)
voluntary eye movement
anterior intraparietal sulcus (AIP)
object-directed grasping
ventral intraparietal sulcus (VIP)
visuomotor guidance
parietal reach region (PRR)
visually guided reach
intraparietal sulcus (cIPS)
object-directed action
monocular blindness
destruction of the retina or optic nerve of onee eyee
bitemporal hemianopia
lesion of medial region of optic chiasm severs crossing fibers; loss of vision of both temporal fields
nasal hemianopia
lesion of laterla chiasm; loss of vision in one of nasal fieelds
homonymous hemianopia
complete cuts of optic tract, lateral geniculate body, or V1; blindness of one entire visual field
macular sparing
damage to the visual cortex spares info from central part of the visual field
scotomas
small blind spots often unnoticed because of nystagmus; brain fills in the blind spots with info from the previous position of the eyes
nystagmus
constant tiny involuntary eye movements
hemianopia affecting the right visual field
a complete lesion of area V1 in the left hemisphere
a large lesion of the lower lip of the calcarine fissure
quadrantanopia that affects most of the upper-right visual quadrant
a smaller lesion of the lower lip of the calcarine fissure
smaller injury (scotoma)
B.K.
V1 damage and scotoma
Patient awoke to discover loss of vision in left visual field
Vision returned to the lower left visual field, but not upper left field
MRI scan revealed evidence of a stroke in the right occipital lope
Perimetry maps regions of blindness by asking patient to detect a small lift moving against a dark background
Shortly after stroke, unable to detect light in the area of the stroke, but could report that it had been there after researchers moved the light to a different part of the visual field (blindsight)
While there’s damage in V1, higher visual areas remain intact
Over time, some vision returned, but the scotoma remained, and form vision was still poor in upper left quadrant
D.B.
V1 damage and blindsight
Had surgery to remove abnormal blood vessels, which removed part of the right calcarine fissure
Patient typically reports they see nothing in left visual field, but sometimes has a feeling that something is there; guess correctly about shape of the object
Accurately indicates the location of stimuli and the orientation of lines they didn’t see
Cortical blindness occurs when a patient has no conscious awareness of visual stimuli, but can accurately indicate location, directions, forms, or colors of the stimuli
fMRRI shows they have activity in V5 when a stimulus is moving in their blind spot, as well as activity in the prefrontal cortex
B.I.
more than blindsight
Child sustained damage to occipital lobe bilaterally in first 2 weeks of life due to a genetic disorder
At age 6, not blind
Can recognize faces, colors, and navigate environment
Significant plasticity to rearrange his visual system and strengthen pathways from subcortical areas to V5
J.L.
V4 damage and loss of color vision
Lost color vision following car accident
Visual acuity improved, but world appeared as shades of gary
Lost ability to remember or imagine colors
Even dreamed in black and gray
P.B.
conscious color perception
Man electrocuted and resuscitated, resulting in significant damage to posterior cortex
Could detect the presence of light, but otherwise blind
retained ability to imagine colors
L.M.
V5 damage and movement
Following damage to area V5, unable to detect motion
Pouring fluids was difficult because she couldn’t see the level rise in the cup
Interacting with people disturbing bc couldn’t see them move
Vision otherwise normal
Case suggest the brain processes the movement of a form separate from the form itself
Symptoms can be mimicked by applying TMS to V5/MT
D.F.
occipital damage and visual agnosia
Patients with CO poisoning leading to damage to area LO have visual form agnosia and can’t recognize line drawings of objects
Patients can’t draw pics of objects when looking at them and can’t reproduce line drawings
No difficulty reaching and grasping objects, even though they can’t recognize them
Unable to correctly judge lines as horizontal or vertical, but can orient movements to match horizontal or vertical lines
Results suggest dorsal stream is intact (guiding movements to a target), but the central stream isn’t (recognizing objects)
visual agnosia
the inability to recognize objects or pictures of objects; or the inabilty to draw a copy of the objects
V.K.
parietal damage and visual guidance
optic ataxia
Associated with damage to posterior parietal lobe
Patient had bilateral strokes in occipito-parietal regions
Normal form and color vision, but couldn't reach for objects or form hand into correct shape to pick up objects
optic ataxia
deficit in visually guided movements like reaching
D and T
higher-level visual processes
D has a lesion to the right occipitotemporal region and has some difficulties reading, but is unable to recognize faces
prosopagnosia
apperceptive agnosia
object agnosia in which the patient fails to recognize a basic feature of the object, such as color or motion
result from bilateral damage to the lateral aspects of the occipital lobe
simultagnosia
patient is able to perceive an object, but unable to perceive more than one object at a time
results form bilateral damage to the lateral aspects of the occipital lobe
associative agnosia
patient can perceive the object, but can’t recognize it
associated with damage to ventral stream
prosopagnosia
can’t recognize familiar faces including their own
rely on recognition based on sound of voice, hair, or way they walk
visual perception normal, and can differentiate between human and nonhuman faces
bilateral damage at the occipitotemporal junction
alexia
inability to read
associated with damage to left fusiform gyrus and lingual area
left hemisphere specialized to combine letters to form words
considered visual agnosia where the patient is unable to combine parts into a whole
cortical blindness
when patient has no conscious awareness of visual stimuli but can accurately indicate location, directions, forms, or colors of the stimuli