Glen Calvin 
Psychology 321
Dr. Morgan
12/3/99
The Visual Cortex

	The area of the human brain which converts light 
energy into a nervous impulse and perceive the world around 
us is known as the visual cortex.  Although the complete 
extent of the human visual cortex is still unmapped, we do 
know that most of the occipital lobe and parts of the 
inferior temporal cortex and posterior parietal cortex 
serve visual functions (Peters 283).  Total size of this 
visual cortex is between 150 and 250 cubic centimeters of 
the 800 cubic cm in each hemisphere (Peters 283).  The 
physical structure of our visual system is both layered and 
columnar, with columns about 2mm deep and 30-100 
micrometers wide (Martin 114).  The human visual system is 
made up of the eye which converts light energy into all or 
none electrical impulses, the optic nerve, which delivers 
this information to the dorsal lateral geniculate nucleus 
of the thalamus (LGN), and the primary visual (striate) 
cortex (Carlson 172).  Also known as Brodmann's Area 17, 
the primary visual cortex is also called the striate cortex 
because it has a distance strip of white matter known as 
the Stria of Genari, which itself is the result of the 
termination of a large number of myelinated axons extending 
from the lateral geniculate nucleus in layer IV (Martin 
114).  This 'optic radiation' from the LGN is approximately 
three millimeters thick (Martin 114).  The LGN projections 
end almost exclusively in the striate cortex, making it a 
'gateway' for visual info to reach the rest of the neo-
cortex (Rose 65). At least 20 subcortical structures and 
nuclei have been identified as projecting information to 
the occipital lobe (Peters 369).  Damage to the parts of 
the visual system connections between the eye and the 
primary visual cortex result in blindness is all or part of 
the visual field (Carlson 172).  
	The primary visual cortex, also abbreviated V1 
(Logothetis 70), which receives information form the visual 
system is located at the back of the brain on the inner 
surfaces of the cerebral hemispheres, primarily on the 
upper and lower banks of the calcarine or 'spur shaped' 
fissure (Carlson 68).  Most inputs to the visual 
association cortex which helps organize and interpret 
visual info, come from the striate cortex (Carlson 171), 
which we now know sends the information on to at least two 
dozen separate cortical regions (Logothetis 70).  In 1982, 
Ungerleider and Mishkin stated that the info received by 
the striate cortex is split in two "streams of analysis", 
one of which flows downward into the inferior temporal 
cortex, and the other which flows up into the posterior 
parietal lobe (Carlson 172).  The roles of these cortexes 
have also been determined, with the ventral, temporal 
cortex stream being responsible for determining 'what an 
object or pattern is', and the dorsal, parietal lobe stream 
recognizing "where an object is located" (Carlson 172).  
Earlier, in 1969, Schnieder called these the 
geniculostriate pathway (for identifying stimuli and 
pattern discrimination), and the retinotectal pathway for 
spatial recognition (Martin 115).  The striate cortex 
projects its axons and information to the extrastriate 
cortex, or visual association areas surrounding it (Carlson 
173).  This 'prestriate' or 'circumstriate' cortex contains 
specialized neurons which respond to specific visual 
information like orientation, motion, spatial frequency, 
retinal disparity, or color (Carlson 173).  
	Because any loss of brain tissue can have dramatic 
effects on brain functioning, it is necessary to continue 
charting the known functions of the human brain.  there are 
now five major approaches to experimental techniques for 
revealing the organization of the visual cortex (Peters 
260).  These include architectonics, the study of cortical 
structure through staining and magnification; connectivity 
patters which map cortical inputs and outputs from cortical 
areas or subcortical nuclei; topographic mapping which uses 
topographically oriented physiological or anatomical 
techniques; physiological functioning which identifies 
visual areas and determines their extent using single unit 
recording PET scans; and behavioral analysis of lesion, 
stimulation, or inactivation effects on an area which 
examines specific changes in visual performance (Peters 261 
264).  Although a functional deficit in behaviour or 
perception after a circumscribed experimental brain lesion 
following a tumor, trauma, or stroke may implement that 
damaged or destroyed area as being necessary for a specific 
function, it does not always indicate 'localization' at 
this specific area (Creutzfeldt 274).  Often, patients who 
have part of their visual cortex surgically removed do not 
at first notice or feel anything (Lausch 73).  Neurosurgeon 
Wilder Penfield wrote "I have found it necessary... to 
remove large areas of cerebral cortex form a patient while 
he was still conscious, using local anesthesia.  As long as 
the brain stem is not molested, the patient remains 
conscious and, curiously enough, is not aware of any 
changes until he turns his attention to a proposition that 
calls for specific use of the removed portion of his 
cerebral cortex" (Lausch 73).  Blindsight phenomenon 
(caused by damage to the PVC or the optic radiations 
leading to it) shows that visual info can control behaviour 
without producing a conscious sensation (Carlson 171).  
Blindsight patients have been known to point to objects in 
the 'blindspots' of their visual field and can determine 
the size and orientation of objects located there, but will 
deny being aware of any object located there (Carlson 172).  
The influence of the amygdalofugal fibers on the visual 
cortex is yet unknown, but it is possible that throughout 
the amygdala, behavioral states could play a role in visual 
info processing in occipital areas (Peters 360).  A lesion 
to a small portion of the human extrastriate cortex in the 
medial occipital lobe (Area V4) can result in loss of color 
vision without interrupting visual focus and sharpness 
(Carlson 174).  This is known as achromatopsia or "vision 
without color", and unless the brain damage is bilateral, 
people will lose color in only half their visual field 
(Carlson 174).  This type of trauma also renders the 
sufferer unable to imagine or remember colors before the 
brain damage (Carlson 174).  Central achromatopsia 
(dyschromatopsia) involves a loss of color vision due to a 
lesion of the visual pathways (optic nerve, chiasm or 
both), and can occur with unilateral inferior occipital 
lobe lesions (Martin 230).  This disorder can affect one 
color more that another, and patients can perform verbal 
tasks related to color, such as correctly answering the 
question "what color is blood?" (an incorrect answer would 
indicate specific color aphasia (Martin 230).  Damage to 
the human visual association cortex can result in visual 
agnosia or "failure to know" (Carlson 177).  There are two 
types of this agnosia, apperceptive, which is a failure in 
'higher perception', and associative agnosia, which is a 
kind of disconnection between the perception and verbal 
areas (Carlson 177).  Bilateral damage to certain areas of 
the association cortex (area V5) can produce agnosia for 
movement such as an inability to judge the speed of a 
moving object (Carlson 181).  While bilateral damage to the 
parieto-occipital border region can cause Balint's 
syndrome, a condition with three types of symptoms (Carlson 
182).  Optic ataxia is a disturbance of hand, eye reaching 
coordination; occular apraxia is an inability to 
systematically scan the contents of a room or picture; 
simultanagnosia is an inability to perceive two different 
objects simultaneously (Carlson 182). An area of complete 
blindness caused by damage to the striatal cortex is called 
a scotoma (Martin 223).  Scotoma which comes from the Greek 
word skotos for dark is misleading because the patient does 
not see blackness, and do not 'see' their scotoma 
(Creutzfeldt 275).  The scotoma is acknowledged when the 
patient bumps into whatever was 'hiding' there.  Lesions to 
the right parietotemporal cortex result in spatial neglect 
disorders where patients ignore entire areas of their field 
of view (Martin 247).  Complete bilateral destruction of 
area 17 in humans causes contical blindness possibly 
leaving the patient only the ability to roughly locate 
bright light sources (Creutzfeldt 276).  Any cooling or 
ablation of striate cortex blocks signals from the 
adjoining and deep layers of the visual cortex (Rose 65).  
A normal, undamaged primate visual system has great 
capacity for recognizing objects regardless of the many 
different images the object may form by changing its size, 
perspective, contrast, color, or even by partial 
obstruction by other visual stimuli (Schiller 342).  The 
extrastriate visual cortex areas serve a complex elaborate, 
and interactive function in the visual process (Schiller 
342).  

Bibliography

Carlson, Neil R.  Psysiology of Behavior 6th edition  Allyn 
and Bacon, Boston, 1998.

Creutzfeldt, O.D.  Cortex Cerebri  Oxford University Press 
inc.,  New York 1995.

Lausch, Erwin  Manipulation Dangers and Benefits of Brain 
Research  The Viking Press, New York 1974.

Logothetis, Nikosk  "Vision a Window on Consciousness"  
Scientific American Vol 281 number 5 November 1999 New York

Martin, Neil G.  Human Neuropsychology  Prentice Hall,  
London. 1999.     
Peters, Alan  Cerebral Cortex vol 3 Visual Cortex  Plenum 
Press, New York 1985.

Rose, David  Models of the Visual Cortex  Jhn Wiley and 
Sons, Chichester, 1985.

Schiller, Peter H.  "Effects of lesions in visual cortex 
area V4 on the recognition of transformed objects"  Nature 
vol 376. No 6538, 27 July 1995.




Lesions of the Occipital Cortex from the Perspective of the 
Neuropsychologist 
Allison Horton

	In order to understand why a neuropsychologist would 
be interested in studying lesions to the occipital cortex, 
one must first have a clear picture of what a 
neuropsychologist is and what they do.  A neuropsychologist 
is a scientist with a Ph.D. in psychology and one who has 
also had specialized training in the principles and 
procedures of neurology, the branch of science dealing with 
the nervous system and its diseases (Carlson 16). The 
purpose of a neuropsychologist's work is to "establish 
relationships between functions such as motor/sensory 
behavior, cognition, perception, mood, emotion and brain 
activity and structure" (Martin 2).  According to J.G. 
Beaumont (an author in this field), neuropsychology is the 
"scientific study of the relationship between the brain and 
mental life" (Martin 3).  Therefore, in order to understand 
the relationships between brain functions and behavior, 
neuropsychologists conduct clinical studies of patients 
with damage to the brain and spinal cord.  Since it is 
clearly unethical to purposely damage a human brain in 
order to observe the effects of the damage, 
neuropsychologists study people who have suffered from 
brain tumors or lesions, strokes, or other trauma to the 
head.  By studying the effects of brain damage on behavior, 
neuropsychologists can determine the different areas of the 
brain that are responsible for certain behaviors.
Neuropsychologists and other researchers have long been 
interested in the functions of the occipital cortex because 
its exclusive purpose involves vision, which is said to be 
the most dominant of the senses.  Although vision is the 
main function of the occipital lobe, other areas of the 
cortex play a role in vision as well because there is no 
specific anatomical division between the occipital, 
temporal, and parietal cortex (Kolb & Whishaw 243).  The 
occipital cortex and its surrounding areas are multi-
faceted and very complex, but with rapid increases in 
technology, new information has been found regarding the 
functions of the occipital cortex and visual systems in 
general.
The occipital lobe (also referred to as the striate cortex, 
Area 17, or V1) is located at the very back of the cerebral 
hemispheres and contains the primary visual cortex.  The 
primary visual cortex receives sensory information from 
different pathways including axons extending from the 
lateral geniculate nucleus (LGN) of the thalamus.  This 
illustrates that the occipital lobe is a complex 
information processing area where input received from the 
eyes travels through specific visual pathways and finally 
ends up in the primary visual cortex where neural 
stimulation is translated into vision.  
It probably isn't too surprising that damage to the 
occipital cortex results in extremely unusual perceptual 
behavior.  Although the primary function of the occipital 
lobe is vision, separate anatomical regions within the 
occipital lobe are involved in the perception of form, 
movement, and color (Kolb & Whishaw 263).  Therefore, if a 
person sustains a lesion to a specific part of the 
occipital lobe, they may lose certain aspects of vision, 
while other parts may remain intact.  It is these changes 
in perception that interest neuropsychologists as they 
study effects of damage to the occipital cortex.
Neuropsychologists and other vision researchers use many 
different techniques to measure the amount of vision that 
has been lost due to damage in certain parts of the visual 
system.  For example, a procedure known as perimetry is 
used to assess a patient's visual field.  During this 
procedure, the patient has one eye covered and the open eye 
staring at a fixed point while a dim light is moved around 
slowly in front of the patient's open eye and the patient 
reports when the spot disappears (Sekuler & Blake 114).  
With this test, the spot would disappear at some point for 
all individuals (not only those who have sustained damage 
to the occipital lobe) because everyone has some blindspots 
on their eyes, but in a person who has a lesion in the 
occipital lobe, the effects would be different.  Small 
lesions in the occipital lobe produce blindspots, known as 
scotomas, but the strange thing is that the patients are 
totally unaware of the defect.  Since the eyes are usually 
in constant motion, other portions of the visual system can 
compensate for the damaged areas and create normal 
perception of the stimulus.  In order to prove to the 
patient that their scotoma is real, the visual system must 
be "tricked" by placing an object directly within the 
blindspot and asking what the object is.  If the patient 
cannot describe the object, it is then moved out of the 
scotoma and suddenly "appears" in the normal region of the 
visual field (Kolb & Whishaw 252).
Another unusual phenomenon that can occur after damage to 
the occipital lobe is visual agnosia.  A patient with 
visual agnosia is "unable to recognize objects or their 
pictorial representations, or to draw or copy them" (Kolb & 
Whishaw 256).  Neuropsychologists studied a 35-year-old 
visual agnosic woman who suffered damage to the lateral 
occipital region from carbon monoxide poisoning.  The woman 
was able to recognize objects, but she couldn't recognize 
drawings of the objects.  In addition, although she could 
draw the objects from memory, she couldn't look at an 
object and draw it, nor could she copy line drawings.  From 
these different assessments, neuropsychologists concluded 
that the woman had serious defects in form perception (Kolb 
& Whishaw 257).
There are many other tests that neuropsychologists use to 
measure the perceptual damage that has occurred as a result 
of an occipital lesion; unfortunately, not much can be done 
to help correct perceptual defects after the damage has 
been done.  However, continual research is useful in 
discovering the different aspects of the brain that are 
responsible for certain behaviors.  Hopefully, someday new 
discoveries will be made to help those who have encountered 
life-altering changes due to severe brain damage.


References:

Carlson, N.  Physiology of Behavior.  Boston: Allyn and 
Bacon, 1998.

Kolb, B. & Whishaw, I.  Fundamentals of Human 
Neuropsychology.  New York: W. H. Freeman and Company, 
1980.

Martin, Neil G.  Human Neuropsychology.  London: Prentice 
Hall, 1999.

Sekuler, B. & Blake, R.  Perception.  New York: McGraw-
Hill, Inc., 1994.




Jeanne Quirk
Psych 321
December 3, 1999

Lesions in the visual cortex from a neurologists view
	
	Of all the senses, vision is the most widely used 
sense by humans. Some 80% of our sensory input is visual, 
it is because of this that much is known about vision.  
More cortex in the human brain is devoted to vision than 
any other function.   The visual cortex primary functions 
are form, location, movement, and color. The visual 
pathways are also resposible for transmitting information 
from the eye to different parts of the brain. There is much 
disagreement amoung neurologists about the exact boundaries 
in the brain of the occipital cortex.  The three clear 
areas involved in vision are the calcarine sulcus, 
calcarine fissure, and the lingual gyrus
	A neurologist is a doctor interested in the diagnosis 
and treatment of disorders of the central nervous system.  
Medical practice is the primary interest of a neurologist 
although a few do research to advance our understanding of 
the biological basis of behavior.  The tools used by a 
neurologist to study lesions of the occipital cortex vary 
according to the disfunction of vision.  A tool used to 
define the  exact areas of loss in the visual field is 
perimetry.  When using perimetry  the patient is asked to 
focus on a black dot on a large white hemisphere while a 
light is moved around the area to define what the patient 
can and cannot see.  Another tool include the placement of 
objects in the part of the visual field that is damaged to 
see if the patient knows they are there without actually 
seeing them.  This is used to decipher whether more 
specific areas of the visual cortex are functioning while 
the lower ones are not, showing the area of the lesion to 
further advance treatment of the patient.  Patients with 
damage to the visual cortex may also be asked to draw 
pictures of objects in front of them and then to draw them 
from memory this tool is  used to define disfunction in 
form perception.  There are many disorders associated with 
lesions to the visual cortex.  The locus and severity of 
the lesion differentiate between disorders, i.e. a 
bilateral lesion will produce a greater loss of the visual 
field.  
	
	 A lesion in one area of the visual cortex will 
produce a loss of one or more of the above named functions.  
The visual cortex is composed of six different regions each 
with its own function, they are known as V1, V2, V3, V3A, 
V4, and V5.  There are also pathways in the visual cortex 
that result in the loss of visual field when lesions occur.  
These pathways are known as the optic nerve, optic chiasma, 
optic tract, and lateral geniculate nucleus. 
	
	V1 or the Striate cortex has a complex heterogeneous 
organization.  The organization of this area was discovered 
using staining for an enzyme, cytochrome oxidase which 
stained blobs in the cortex for different functions, color 
perception, and form and motion perception respectively.  
Lesions to this area result in the loss of cognition of 
visual stimuli.  Patients act as though they are blind but 
tests show the visual stimuli can get to higher pathways 
i.e., the LGN and V2 without the patient actually seeing 
the object but 'feeling' where or what it is. This 
phenomenon is called cortical blindness, no actual 
cognition of the visual stimuli but the ability to report 
the location to the stimuli. This proves that the striate 
cortex is needed to function for the perception to get to 
higher levels, color, movement, and form.  
	
	V2 is also heterogeneous in function but organized 
differently than V1.  The striate cortex is organized in 
areas of blobs whereas V2 is organized in many layers.  The 
idea is the same for both areas they just have different 
ways of processing information.  One type of layer is for 
color perception and the other layer is for form and 
movement.  This may be an evolutionary advantage, a damage 
to one of these areas does not result in the complete loss 
of visual input and perception.  
	
	V3, V4, and V5 have more specialized functions than V1 
and V2, therefore lesions to these areas produce more 
specific loss of vision.  A lesion in V3 will result in 
some loss of form, the shape of an object in motion or the 
ability to locate an object.  Some cases only lose the 
ablitiy to see an object in motion, some only lose the 
ability to locate an object.  This shows that the visual 
cortex analyzes movement of form differently from location 
of a form.  Loss of color sight and recognition results 
from a lesion to V4.  These patients see everything in 
shades of grey and can eventually lose all memory of color 
and the ability to imagine color. Proving that these 
functions are dependent on some of the occipital cortex.  A 
lesion in V5 of the visual cortex results in the loss of 
the ability to perceive objects in motion.  The patient can 
focus on still objects but when the object is in motion it 
just disappears. 

	Lesions in the cortex are not the only lesions that 
can result in the loss of vision.  Disorders of visual 
pathways can also result in the loss of vision in a certain 
portion  of the visual field.   A lesion on the optic nerve 
results in the loss of vision in the eye associated with 
that nerve or monocular vision.  Hemianopia or the partial 
loss of vision in the opposite halves of visual fields both 
eyes results from a lesion to the optic chiasm.  The area 
of loss in the visual field depends on the locus of the 
lesion on the optic chiasm.  A lesion in the optic tract 
causes a disorder known as homonymous hemianopia, or the 
loss of vision in half the visual field for each eye.  The 
central area of the visual field is preserved in these 
disorders, the reason for this is unknown.  One current 
theory is that the central region received twice as much 
blood from two different arteries, and the other theory is 
that the fovea of the retina projects to both areas even if 
one occipital lobe is damaged the other recieves 
information from the fovea.  Small blindspots in the visual 
field that often go unnoticed are called scotomas. These 
blindspots are a result of a lesion to the occipital  
cortex.  They often go unnoticed  by patients because the 
eye constantly corrects for the missing visual information 
by moving around the area of loss to perceive the whole 
image.

	Visual agnosia is a visual disorder that results from 
bilateral damage to the lateral occipital region, usually 
caused by carbon monoxide poisoning.  This disorder is 
characterized by the inability to recognize or draw objects 
themselves or their pictoral representations. Some cases 
result in the inability to draw objects from memory but can 
guide hand movements toward objects that could not be 
percieved.  A similar disorder, optic ataxia, results in 
the opposite.  The patient cannot guide hand movements for 
different objects.  These two disorders, taken together 
show that perception of object form is completely different 
from visually guided hand movements.  Both of these 
disorders results from lesions to the bilateral occipital 
lobes. 

	Two more disorders resulting from occipital-temporal 
lesions are prosopagnosia, the inability to recognize faces 
and alexia, the inability of read.  Prosopagnosia results 
from a lesion to the right occipital-temporal lobe.  The 
severity of this disorder can extend to the inability of 
the patient to recognize their own face in the mirror. Many 
patients can process information from faces such as 
lipreading or imitate facial expressions.  Alexia results 
from a lesion to the left occipital-temporal region.  These 
two disorders together show that face identification and 
picking out speech information do not use the same area of 
the brain, or that the two areas are asymetrical.  

	The visual cortex as a whole serves a variety a 
purposes for humans.  We use more visual stimuli than any 
other sensory input.  The breakdown of the occipital lobe 
specifies a variety of functions, form, movement, and 
color.  Our ability to see our environment is one of the 
reasons humans are so interesting. No other animal has the 
accuracy of vision or the amount of brain space given to 
vision.  We are still learning what some of the specific 
functions of the occipital cortex are. These findings will 
one day help us treat blindness in the future. 
 
Kolb, B. and Whishaw, I. Fundamentals of Human 
Neuropsychology. New York: W.H. Freeman and Company, 1980

Dimond, Stuart J, Neuropsychology, Boston, 1980.

Carlson, Neil R., Physiology of Behavior, Boston 1998




Eliana Machuca
Psychology
12-3-99
Occipital Cortex Lesion
From the prospective of
The Patient
	About a year ago I had an accident in which I fell 
backwards onto a sharp piece of metal.  The metal pierced 
the back of my head.  It went all the way to my brain.  I 
guess I'm lucky to be alive.  It struck a region of my 
brain called the occipital lobe or visual cortex.  The 
Occipital cortex has many different subdivisions that 
perform different operations but work together to allow for 
vision.  The region that I damaged is labeled V4. I'm am 
very lucky that I didn't damage any other area as well.  My 
accident could have been much worse.
	Now, because of the damage I have done to the V4 area 
of my occipital lobe.  I am only able to see in shades of 
gray.  I can't think about color or imagine what it looks 
like. I also don't remember what colors used to look like 
before I had my accident. (Kolb 274).  Sometimes it makes 
me very sad.  One of my very favorite things to do with my 
children was to take them out at dusk and watch the sunset.  
I still take them, but for me it is definitely not the same 
experience.  I remember how it made me feel, the awe and 
wonder of such a miraculous sight.  But I don't remember 
why it was so miraculous any more.  Some times I don't even 
want to eat, because food looks so gross and dead. I 
usually close my eyes when I'm eating.  At least my husband 
doesn't have to worry about me having roaming eyes, most 
people just look pasty and gray, not attractive at all 
(Kolb 256).
	Thing could have been worse.  Sometimes I tell myself 
that to make me feel better. Many other parts of that 
region of my brain could have been damaged.  While I was in 
the hospital there were other patients that also had 
occipital lobe damage.  Each of them with there owns story 
and their own disorder.
	One woman developed visual agnosia.  She could still 
see every thing and she could see in color, but when she 
saw an object she couldn't recognize its character or 
meaning.  If she saw a chalk board eraser she wouldn't be 
able to tell you what it was, show you how to use it, or 
even remember seeing it before.  But if she could smell or 
feel the chalk board eraser she would be able to tell you 
what it was.  It was the same way with taste and sound.  If 
she could taste or hear the object then she would be able 
to recognize what it was.  She was still able to read and 
write and she could recognize pictures of her friends and 
family. (Gilinsky 291)
There was another guy in the hospital that had another kind 
of visual agnosia.  His was called prospagnosia.  This 
happened because he damaged the area below the region of 
the brain call the calcarine fissure where the occipital 
and temporal lobes meet. (Kolb 260) He couldn't recognize 
faces of his friends and family or distinguish between new 
faces he would come across. (Joynt 53)  He even had trouble 
recognizing his own face in the mirror.  That would be so 
scary and confusing for me.  I know it was for him because 
he made us all do our hair a different way unless we had a 
mustache or a characteristic birthmark.  If we didn't have 
any of these things he would be at a complete loss (Kolb 
260).
The doctors said I was lucky that the piece of metal didn't 
pierce any deeper that it did, because it came close to 
hitting the V5 area of my occipital lobe.  If that happened 
I wouldn't be able to see objects while they were moving.  
I would be able to see them when they were still but as 
soon as they moved they would vanish or seem to be frozen 
(Kolb 247).  This is what happened to who became my best 
friend at the hospital.  It was very distressful for her 
and even scarier than not being able to recognize people's 
faces.  If there were people walking around in the room 
with her in it people would suddenly appear to be "here or 
there".  She couldn't see them while they moved around.  At 
times it felt to her like every one was sneeking up on her.  
We all tried to stay very still while we were around her.  
It was also very hard for her to do things as simple as 
pouring a glass of juice.  She said "the fluid appeared to 
be frozen and she could not stop pouring because she could 
not see the fluid level rise."  
I think the worse thing that could have happened would have 
been damaging the V1 area of my occipital lobe.  If that 
happened I would technically still be able to see but I 
wouldn't be able see what I was seeing.  What happens is 
that the even though visual imput can still get to higher 
brain levels It gets disturbed in the V1 area.  The V1 area 
of the brain sends information to many other areas of the 
occipital lobe.  It is like the first stop in the occipital 
lobe for vision (Kolb 247).  Apparently a person with 
damage to this area would still be able to act on visual 
information and even be able to point to an area where a 
spot of light was turned on.  But if you asked that person 
what they say they would say "nothing". (Kolb 255)
At least I can still see something.  After a year with this 
disorder I am starting to get used to it.  It's not like I 
can say that I miss seeing in color, because I can't even 
ember what I'm missing.  Anyway, like I said, it could 
be worse.

References

Gilinsty, S.A. Mind and Brain Principles of Neuropsychology 
New York: Praeger. 1884 pgs.290-293

Joynt, J.R Occipital Lobe Syndromes Handbook of clinical 
Neurology, Vol.1 Elsevier Science Publishers B.V. 1985 

Kolb, B. and Whishaw, I. Fundamentals of Human 
Neuropsychology. New York: W.H. Freeman and Company, 1980

Copyright © 1995, Dr. John M. Morgan, All rights reserved - This page last edited December 13, 1999
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