Occipital Cortex

by John Lenahen


The occipital cortex is at the back of the brain and 
contains the visual cortex which processes visual input.
This article will look at lesions that have damaged the
occipital cortex in order to provide treatment for
intractable epilepsy, leading to impaired visual implicit
memory for words, and  bilateral occipital cortex
ischemia, setting the stage for Anton's syndrome. Lesions
to the occipital cortex and the relation to Balint's
syndrome will be looked at along with the effects it has
on patients behavior.The neuroanatomy  of the occipital
cortex will be discussed to give the reader a better
understanding of this particular brain area. How lesions
affect a persons behavior will be discussed including how
the neural interactions of other brain areas play a part
in the persons behavior. Finally, how these behavioral
changes are diagnosed using neuropsychological tests will
be discussed along with adaptations the patient must make
to the changes in their behavior upon suffering occipital
cortex lesions.
    In the caudal region of the brain, lies the occipital 
 lobes. The primary visual cortex lies at the posterior
end of the occipital lobes along the calcarine fissure,
mostly hidden between the two cerebral hemisphere. It
receives visual information (Carlson, 1994). It is the
axons of the retinal ganglion cells that bring the visual
information to the rest of the brain. These axons ascend
through the optic nerves until they reach the dorsal
lateral geniculate nucleus (DLGN) of the thalamus. Six
layers of neurons within the thalamus each receive input
from only one eye. The two inner layers that contain
larger cell bodies than the remaining four is called the
magnocellular layers which respond best to coarse moving
objects. The outer four layers are called the
parvocellular layers which responds well to color
differences and to finer stationary patterns. These
layers are responsible for the analysis of visual
information. The neurons of the DLGN then send their
axons via the optic radiation's to the primary visual
cortex (Carlson, 1994).
    The axons from ganglion cells from the inner halves
of the retina cross at the optic chiasm and ascend to the
DLGN nucleus of the opposite side of the brain. The axons
leaving the outer side of the retina do not cross at the
optic chiasm and remain on the same side of the brain.
Each hemisphere of the brain receives visual information
from the contralateral half of the visual scene (Carlson,
1994).Any damage to a portion of the occipital lobe
produces a blindspot in the contralateral visual field
(Sdorow, 1993).
    The neural scheme of shape detectors being built out
of detectors of lines of different orientation and
length, is an unknown process ( Winson, 1985). Winson has
stating, "The anatomical area in which it culminates may
be the inferotemporal cortex. Much as the primary visual
cortex sends inputs to adjacent feature detection areas,
so these areas send inputs to the inferotemporal region"
(1985, p.25-26). The neurons in this area respond to
visual stimuli yet not to any other sensory inputs.
Winson (1985) states, "If a neuron in the inferotemporal
cortex were to fire in response to the particular shape
of an object, it would do so regardless of where the
object appeared within the broad region of the visual
field" (p.26). The inferior temporal cortex is located on
the ventral part of the temporal lobe. The recognition of
visual patterns and identification of particular objects
takes place in this region, along with the analyses of
form and color and the perceptions of 3-D objects and
backgrounds. It consist of two major regions called the
TE and TEO (Carlson, 1994).
    Inhibitory cells in the LGN release an inhibitory
transmitter chemical called GABA, which have a strong
control over the transfer of information the cells
receive that pass on information to the visual cortex.
They also play a major role in the restriction of the
development of excitatory responses in the cortical
network (Sillito, 1995). Sillito (1995) states, "cortical
processes utilizing the inhibitory transmitter GABA
contribute to response properties of visual cortical
cells which link to visual perception" (p.304). The
brainstem  has inputs from its neuromodulatory systems to
the visual cortex which involve noradrenaline,
acetylcholine, and serotonin as neurotransmitters. ACh is
known to facilitate excitatory interneurons in the visual
cortex and directly excites inhibitory interneurons
(Sillito, 1995). Sillito (1995) has stated, "The
cholinergic system, in combination with other
neuromodulatory inputs, determines the change in the
brain mechanisms linked to behavioral state, for example
between the response of a sleeping and waking cortex. If
the cholinergic input to the cortex is damaged, one could
expect highly impaired cortical function" (p.305).
    Anton's syndrome refers to the clinical phenomenon of
the denying of blindness in a patient who has suffered
acquired cortical blindness. The most common situation in
which this occurs is acute bilateral occipital cortex
ischemia secondary to posterior circulation insufficiency
(McDaniel, K.D., McDaniel, L.D., 1991). Some
investigators have stated that the denial of blindness
results when occipital cortex lesions go beyond the
calcarine cortex to include visual association cortices.
Patients with Anton's syndrome have been frequently
observed to have disorders of recent memory. This
disorder is produced from cortical blindness being
frequently secondary to posterior circulation
insufficiency, the inferomedial temporal lobe structures
can also be similarly affected, creating the disorder in
recent memory (McDaniel and McDaniel, 1991). McDaniel and
McDaniel (1991) has stated, "numerous case reports of
Anton's syndrome occurring in patients with lesions to
the anterior visual system. In all cases of Anton's
syndrome associated with anterior visual system lesions,
except perhaps one, there has been evidence of profound
diffuse cognitive dysfunction" (101). They continue by
saying that these patients show evidence of "coarse brain
disease", which includes clouding of consciousness,
confusion, disorientation, and severe dementia (McDaniel
and McDaniel, 1991). EEG recordings of an unconscious
patient showed an episode of rhythmic sharp wave activity
in the left occipital area which lasted for 5 minutes.
This was later followed in the same recording by an
episode of high amplitude sharp wave discharges occurring
in the right posterior temporal and occipital areas.
After the patient regained consciousness, she had Anton's
syndrome ( Roos, Tuite, Below, Pascuzzi, 1990). These
studies show the effects lesions in the occipital cortex
have on patients behavior upon acquiring Anton's
syndrome.
     Balint's syndrome is the classification used for
patients visually disoriented and who have poor skills
reaching to objects under visual guidance. Balint's
syndrome patients may also have problems disengaging
attention. Patients with Balint's syndrome did worse than
the control groups when asked to detect the presence of
two targets in a color plus size condition. The results
of this study showed that the patients can orient to
information that is computed in parallel across a visual
display. The problems with patients suffering Balint's
syndrome arise when they have to disengage their
attention from one target in order to detect another
(Humphreys, 1995). They further extend the importance of
disengagement problems in Balint's syndrome by claiming
it can account for a wide range of the phenomena
associated with the syndrome. They exclaim that
difficulties patients have with copying can be connected
to their problems in moving attention across a figure in
order to allow accurate reproduction. The difficulties
they experience in identifying objects can be attributed
to their attention being captured at times by a local
part of an object, which they will then take as the whole
(Humphreys, 1995). 
    (Benson et al, 1988) has stated, after observing four
patients who developed a full Balint's syndrome, that
when features of Balint's syndrome are present, there is
an implication of a bilateral parieto-occipital
pathological condition. In their study of five patients,
four of them developed Balint's disease, which was
determined due to the fact they developed a strong
tendency to fix their gaze on a single object (sticky
fixation), an inability to touch a stationary object held
out in front of them (ocular dysmetria), and routinely
failed to find all objects in an array (simultagnosia).
The patients displayed predominant parieto-occipital
atrophy on both computed tomography, and magnetic
resonance imaging. In one patient who had a battery of
neuropsychological tests done, demonstrated visually
oriented impairments reflected in a 22-point difference
in verbal (VIQ) and performance (PIQ) subscores. The CT
scan reading was normal, but the patients EEGs were
abnormal, displaying generalized slowing and disorganized
background frequencies. Gerstmann's syndrome and Balint's
syndrome were present. After repeated CT and MRI scans
were done, they revealed atrophy in great amounts in the
occipital and parietal regions bilaterally. There was no
evidence of mass lesions or focal lucency (Benson et al,
1988).
    Perceptual (visual implicit memory, conceptual
implicit memory, and explicit memory), was observed in a
patient M.S., who had a large lesion in the right
occipital lobe. He had most of his right occipital lobe
removed for the treatment of what would have been
intractable epilepsy (Gabrieli et al., 1995). He has
continued to be seizure free and adapts well in society
as an owner of a computer software company. M.S. scored a
110 on the Wechsler Adult Intelligence Scale-Revised and
a General Memory score of 119 Wechsler Memory/
Scale-Revised. He had a score of 92 on the Attention
Concentration index (Gabrieli et al., 1995). The study
compared him with 5 normal, male controlled subjects, 2
amnesia patients, and 7 patients with focal cortical 
lesions not invading the right occipital cortex. Specific
association between the right occipital lesion and
impaired perceptual-identification priming is supported
in the article by the intact priming shown by other
focal-lesion patients. As a group excluding M.S., they
showed priming by requiring shorter duration's to
identify studied versus baseline words. M.S. had no
problem identifying baseline words, but showed no
priming, and was slightly superior for identifying
baseline compared to studied words. His explicit memory
for words was unimpaired, since his recognition accuracy
was similar to the mean of the control and focal lesion
subjects. He also showed a normal magnitude of priming
after his exposure to auditory words, yet he failed to
show an increased priming after visual exposure to words.
This performance indicates there is a selective deficit
in visual priming, and his nonvisual word-completion
priming remained intact (Gabrieli et al., 1995). 
    (Gabrieli et al., 1995) concluded from the study,
"M.S., a patient with right-occipital lesion, showed a
novel pattern of intact and impaired memory: a) intact
performance on explicit tests of recognition and cued
recall, b) intact performance on an implicit test of
conceptual memory, and c) impaired performance on
implicit tests of visual perceptual memory. He thus
showed a specific deficit in visual implicit memory"
(p.80). They finish the article by concluding that the
studies done with M.S. suggest that there is a memory
system that can record, retain, and retrieve recent
visual experience that enhances perceptual performance in
human vision, located in the right occipital lobe. Also
stated is the fact that the memory in this system is
independent from any other forms of memory which make it
possible for humans to recall or recognize their
experiences in vision (Gabrieli et al., 1995).
   The Gabrieli et al. study, expresses the importance
the occipital lobes have on human behavior. Along with
the other studies stated in this article, we can see that
the occipital lobes are not only important for vision,
but certain forms of memory and attention each having an
affect on human behavior.



References:
Benson, B. F., & Davis, J.D., & Synder, B. D. (1988).
Posterior Cortical Atrophy. Archives of Neurology, 45,
789-793.

Carlson, N. R. (1994). Physiology of Behavior. 5th ed.
MA: Paramount Publishing.

Gabrieli, J. D. E., & Fleischman, D. A., & Keane, M. M.,
& Reminger, S. L., & Morrell, F. Double Dissociation
Between Memory Systems Underlying Explicit and Implicit
Memory In The Human Brain. Psychological Science, 6(2),
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Humphreys, G.(1995). When paying attention is too costly.
In Gregory, R., & Harris, J., & Heard, P., & Rose, D. The
Artful Eye (pp. 125-140). Oxford: Oxford University
Press.

McDaniel, K. D., & McDaniel, L. D. (1991). Anton's
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101-105.

Roos, K. L., & Tuite, P.J., & Below, M. E., & Pascuzzi,
R. M. (1990). Reversible cortical blindness (Anton's
syndrome) associated with bilateral occipital EEG
abnormalities. Clinical Electroencephalogram (DCG),
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Sdorow, L. M. (1993). Psychology. 2nd ed. Iowa: Wm. C.
Brown Communications, Inc.

Sillito, A. (1995). Chemical soup: where and how drugs
may influence visual perception. In Gregory, R., &
Harris, J., & Heard, P., & Rose, D. The Artful Eye (pp.
294-310). Oxford: Oxford Press.

Winson, J. (1985). Brain and Psyche. Garden City: Anchor
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Copyright © 1997, Dr. John M. Morgan, All rights reserved - This page last edited March 17, 1997
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