Transcript localization

LOCALIZATION
By: Jafar Mehvari, MD
Neurologist and Epileptologist
Associative Professor of Isfahan University
of Medical Science
General Anatomic and Physiologic
Considerations of Cortical Function
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Along strictly histologic lines, Brodmann
distinguished 47 different areas of cerebral cortex
the cortex as a heterogeneous array of many
anatomic systems, each with highly organized
intercortical and diencephalic connections.
it has a surface extent of about 4000 cm2—about
the size of a full sheet of newsprint (right and left
pages).
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Contained in the cortex are many billions of neurons
(estimated at 10 to 30 billion) and five times this
number of supporting glial cells.
Most of the human cerebral cortex is
phylogenetically recent, hence the term neocortex
allocortex (“other cortex”), which comprises mainly
the hippocampus and olfactory cortex
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Histology of the neocortex, six layers (laminae) can be
distinguished
the molecular (or plexiform), external granular, external
pyramidal, internal granular, ganglionic (or internal
pyramidal), and multiform (or fusiform) layers
Two main types of neocortex are recognized: (1) the
homotypical cortex, in which the six-layered
arrangement is readily discerned, and
(2) the heterotypical cortex, in which the layers are less
distinct
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The association cortex—the large areas (75
percent of the surface) that are not obviously
committed to primary motor or sensory functions—is
generally of this latter type.
precentral cortex (Brodmann’s areas 4 and 6,
mainly motor regionis dominated by pyramidal
rather than granular cells, especially in layer V
(hence the term agranular
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primary sensory cortex—postcentral gyrus (areas 3,
1, 2), banks of the calcarine sulcus (area 17), and
the transverse gyri of
Heschl (areas 41 and 42)—where layers II and IV
are strongly developed for the receipt of afferent
impulses, has been termed granular cortex
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certain regions of the cerebrum are committed to
special perceptual, motor, sensory, mnemonic, and
linguistic activities,
 In area 17, the polar region of the occipital lobe,
there are discrete, highly specialized groups of
neurons, each of which is activated in a small area
of lamina 4 by spots of light or lines and
transmitted via particular cells in the lateral geniculate
bodies;
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other groups of adjacent cortical neurons are
essential for the perception of color
between the main unimodal receptive areas for
vision, audition,and somesthetic perception are
zones of integration called heteromodal cortices
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Cortical-subcortical integrations
Interregional connections
Disconnection syndromes depend not merely on
involvement of certain cortical regions butalso on
the interruption of inter- and intrahemispheric fiber
tracts
the involved fiber systems include the corpus
callosum, anterior commissure, uncinate
temporofrontal fasciculus, occipito- and
temporoparietal tracts
SYNDROMES CAUSED BY
LESIONS OF THE FRONTAL
LOBES
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30 percent of the cerebrum
Brodmann’sareas 4, 6, 8, and 44 relate specifically
to motor activities
primary motor cortex, i.e., area 4, is directly
connected with somatosensory neurons of the
anterior part of the postcentral gyrus as well as
with other parietal areas, thalamic and red nuclei,
and the reticular formation of the brainstem.
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Area 8 is concerned with turning the eyes and head
contralaterally.
Area 44 of the dominant hemisphere (Broca’s area)
and the contiguous part of area 4 are “centers” of
motor speech and related functions of the lips, tongue,
larynx, and pharynx
The medial-orbital gyri and anterior parts of the
cingulate gyri, which are the frontal components of the
limbic system, take part in the control of respiration,
blood pressure, peristalsis, and other autonomic
functions
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all motor activity requires sensory guidance, and
this comes from the somesthetic, visual, and auditory
cortices and from the cerebellum via the ventral tier
of thalamic
The most anterior parts of the frontal lobes (areas 9
to 12 and 45 to 47), sometimes referred to as the
prefrontal areas,
initiation of planned action and executive control of
all mental operations, including emotional
expression.
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The frontal agranular cortex (areas 4 and 6) and,
more specifically, pyramidal cells of layer V of the
pre- and postcentral convolutions provide most of
the cerebral efferent motor system that forms the
pyramidal or corticospinal tract
Areas 8 and 6 are connected with the ocular and
other brainstem motor nuclei and with identical
areas of the other cerebral hemisphere through the
corpus callosum.
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Electrical stimulation of the orbitofrontal cortex and
cingulate gyrus has manifest effects on respiratory,
circulatory, and other vegetative functions, as
already mentioned.
Clinical Effects of Frontal Lobe
Lesions
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(1) motor abnormalities related to the prerolandic motor cortex
; (2) speech and language disorders related to the dominant
hemisphere;
(3) incontinenceof bladder and bowel
; (4) impairment of certain cognitiv functions, especially attention,
concentration, capacity for sustained mental activity, and ability to
shift from one line of thought or action to another—i.e., bot
impersistence and perseveration;
(5) akinesia and lack of initiative and spontaneity (apathy and
abulia);
(6) other changes in personality, particularly in mood and selfcontrol
(disinhibition of behavior); and
(7) a distinctive abnormali tof gait
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Destruction of Broca’s convolution (areas 44 and
45) and the adjacent insular and motor cortex of
the dominant hemisphere result in a reduction or loss
of motor speech, and agraphia, and apraxia of the
face, lips, and tongue
Damage to the cortices anterior to areas 6 and 8—
i.e., to areas 9, 10, 45, and 46—the prefrontal
cortex, and also the anterior cingulate gyri, has less
easily defined effects on motor behavior
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An ataxia of the contralateral limbs has been
attributed to prefrontal lesions, but careful anatomic
verification is lacking
the resultant pattern is a slowed, slightly
imbalanced, and short-stepped gait with the torso
and legs not properly in phase when placed in
motion, to which may be added the feature of
“magnetic” gait,
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In many instances
with frontal lobe lesions are inclined to manipulate
objects placed before them (utilization behavior) or
to imitate the gestures of others. extreme degrees of
hyperactivity (“organic drivenness”) bilateral
lateralorbital lesions
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Incontinence is another manifestation of frontal lobe
disease. Right- or left-sided lesions involving the
posterior part of the superior frontal gyrus, the anterior
cingulate gyrus
speech and language, a number of abnormalities other
than Broca’s aphasia appear in conjunction with disease
of the frontal lobes—laconic speech, lack of
spontaneity of speech, telegraphic speech
(agrammatism), loss of fluency, perseveration of speech,
a tendency to whisper instead of speaking aloud, and
dysarthria.
Cognitive and Intellectual Changes
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the frontal lobes are injuredby disease, there was
not only a general psychomotor slowing and easy
distractibility but also an erroneous analysis of the
abovelisted conditions of the problem.
“loss of the abstract attitude” (the patient thinks
concretely, i.e., he reacts directly to the stimulus
situation
Other Alterations of Behavior and
Personality
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A lack of initiative and spontaneity is the most
common effect of frontal lobe
they tend to perseverate.
Placidity is a notable feature of the behavior
Worry, anxiety, self-concern, hypochondriasis,
complaints of chronic pain, and depression are all
reduced by frontal lobe disease
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Extensive and bilateral frontal lobe disease is
accompanied by a quantitative reduction in all
psychomotor activity
The number of movements, spoken words, and
thoughts per unit of time diminish.
Abulia
akinetic mutism
bilateral lesions in the ventromedial frontal regions
or frontal diencephalic
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hyperactivity syndrome,or “organic
drivenness,”combined frontal and temporal lobe
lesions,
Some patients, particularly those with inferofrontal
lesions, feel compelled to make silly jokes that are
inappropriate to the situation—so-called
Witzelsucht or moria
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patients with lesions of either frontal lobe manifest
a slight elevation and instability of mood, with
increased talkativeness and a tendency to joke, lack
of tact, inability to adapt to a new situation, and
loss of initiative
More right
temporal
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Most of the temporal lobe cortex, including Heschl’s
gyri, has nearly equally developed pyramidal and
granular layers
Unlike the six-layered neocortex, the hippocampus
and dentate gyrus are typical of the
phylogenetically older three-layered allocortex.
inferior or uncinate fasciculus connects the anterior
temporal and orbital frontal regions
The arcuate fasciculus connects the posterosuperior
temporal lobe to the motor cortex and Broca’s area
Clinical Effects of Temporal Lobe
Lesions
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Visual Disorders
that lesions of the white matter of the central and
posterior parts of the temporal lobe
characteristically involve the lower arching fibers of
the geniculocalcarine pathway (Meyer’s loop).
upper homonymous quadrantanopia
Visual hallucinations of complex form, including ones
of the patient himself (autoscopy), appear during
temporal lobe seizures large (macropsia) or small
(micropsia), too close or far away, or unreal
Cortical Deafness
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Bilateral lesions of the transverse gyri of Heschl,
while rare, are known to cause a central deafness
cortically deaf persons may seem to be unaware of
their deafness, a state similar to that of blind
persons who act as though they could see (the latter
is called Anton syndrome
they are heard less well in the ear contralateral to
the lesion.
areas 41 and 42).
Word-Deafness (Auditory Verbal
Agnosia
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Lesions of the secondary (unimodal association)
zones of the auditory cortex—area 22 and part of
area 21—
have no effect on the perception of sounds and
pure tones
inability to recognize sounds, different musical notes
(amusia), or words
In agnosia for sounds, auditory sensations cannot be
distinguished from one another
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Amusia proves to be more complicated, for the
appreciation of music has several aspects: the
recognition of a familiar melody and the ability to
name it (musicality itself); the perception of pitch,
timbre, and rhythm; and the ability to produce, read,
and write music.
results from lesions in the middle temporal gyrus and
not from lesions at the pole of the temporal lobe
In any case, the temporal lobe opposite that responsible
for language (i.e., the right) is implicated in almost all
cases
Word-Deafness (Auditory Verbal
Agnosia
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Worddeafnes is a failure of the left temporal lobe
function in decoding the acoustic signals of speech
and converting them into understandable words.
can occur by itself, without other features of
Wernicke’s aphasia verbal agnosia may be
combined with agnosia for sounds and music, or the
two may occur separately
Auditory Illusions
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sounds are perceived as being louder or less loud
than normal
Sounds or words may seem strange or
disagreeable, or they may seem to be repeated, a
kind of sensory perseveration.
Elementary hallucinations and dreamy states have
been reported with
lesions of either temporal lobe
Auditory Hallucinations
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Elementary
Complex
sounds and musical themes are heard more clearly
than voices
the superior and posterior parts of the dominant or
both temporal lobes were then involved
Vestibular Disturbances
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In the superior and posterior part of the temporal
lobe (posterior to the primary auditory cortex
If this area is destroyed on one side, the only clinical
effect may be an illusion that the environment is
tipped on its side or is upside down
Epileptic activation of this area induces vertigo or a
sense of disequilibrium
Disturbances of Time Perception
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In a temporal lobe seizure originating on either
side, time may seem to stand still or to pass with
great speed.
Certainly the most common disruptions of the sense
of time occur as part of confusional states of any
type
The patient with a Korsakoff amnesic state is unable
to place events in their proper time relationship
Disturbances of Smell and Taste
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seizure foci in the medial part of the temporal lobe
(in the region of the uncus) often evoke olfactory
hallucinations
posterior orbitofrontal, subcallosal, anterior
temporal, and insular cortices,
Stimulation of the posterior insular area elicited a
sensation of taste along with disturbances of
alimentary function
Other (Nonauditory) Syndromes
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Amnesic dysnomia
Prosopagnosia The loss of certain visual integrative
abilities, particularly face recognition
Disorders of Memory, Emotion, and
Behavior
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Attention must be drawn to the central role of the
temporal lobe, notably
its hippocampal and limbic parts, in memory and
learning and in
the emotional life of the individual.
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I. Effects of unilateral disease of the dominant temporal lobe
A. Homonymous upper quadrantanopia
B. Wernicke’s aphasia (word-deafness—auditory verbal
agnosia)
C. Amusia (some types)
D. Impairment in tests of verbal material presented
through the auditory sense
E. Dysnomia or amnesic aphasia
F. Visual agnosia
G. Occasionally amnesic (Korsakoff) syndrome
II. Effects of unilateral disease of the nondominant temporal
lobe
A. Homonymous upper quadrantanopia
B. Inability to judge spatial relationships in some cases
C. Impairment in tests of visually presented nonverbal material
D. Agnosia for sounds and some qualities of music
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III. Effects of disease of either temporal lobe
A. Auditory, visual, olfactory, and gustatory
hallucinations
B. Dreamy states with uncinate seizures
C. Emotional and behavioral changes
D. Delirium (usually nondominant)
E. Disturbances of time perception
IV. Effects of bilateral disease
A. Korsakoff amnesic defect (hippocampal formations)
B. Apathy and placidity
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SYNDROMES CAUSED BY LESIONS OF THE
PARIETAL LOBES
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The postcentral gyrus, or primary somatosensory
cortex, receives most of its afferent projections from
the ventroposterior thalamic nucleus, which is the
terminus of the ascending somatosensory pathways.
The primary sensory cortex projects to the superior
parietal lobule (area 5), which is the somatosensory
association cortex
Clinical Effects of Parietal Lobe
Lesions
Cortical Sensory Syndromes
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an impairment or loss of the sense of position and
passive movement and the ability to localize tactile,
thermal, and noxious stimuli applied to the body surfa
to distinguish objects by their size, shape, and texture
(astereognosis)
to recognize figures written on the skin;
to distinguish between single and double contacts (twopoint discrimination
and to detect the direction of movement of a tactile
stimulus.
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With anterior parietal lobe lesions there is often an
associated mild hemiparesis, since this portion of the
parietal lobe contributes a considerable number of
fibers to the corticospinal tract
weakness, tend to remain hypotonic and the
musculature may undergo atrophy of a degree not
explained by inactivity alone
The Asomatognosias
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The term asomatognosia denotes the inability to
recognize part of one’s body
asomatognosia
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with a dense hemiplegia, usually of the left side, may
be indifferent to the paralysis or unaware
If told it is paralyzed, the patient may deny that this is
so or offer an excuse:
cortex and white matter of the superior parietal lobule
Unilateral asomatognosia is seven times as frequent
with right (nondominant) parietal lesions as with leftsided ones
Often there is a blunted emotionality
the right parietal lobe is truly dominant
Gerstmann Syndrome
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The characteristic features are inability to designate or
name the different fingers of the two hands (finger
agnosia),
confusion of the right and left sides of the body,
and inability to calculate (dyscalculia)
to write (dysgraphia).
One or more of these manifestations may be associated
with word-blindness (alexia) and homonymous
hemianopia or a lower quadrantanopia,
lesion is in the inferior parietal lobuleparticularly the
angular gyrus or subjacent white matter of the left
hemisphere
Ideomotor and Ideational Apraxia
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patients with parietal lesions of the dominant
hemisphere who exhibit no defects in motor or
sensory function lose the ability to perform learned
motor skills on command or by imitation
Visual Disorders with Parietal Lesions
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A lesion deep to the inferior part of the parietal
lobe, at its junction with the temporal lobe, involves
the geniculocalcarine radiations and result in an
incongruous homonymous hemianopia or an inferior
quadrantanopia
An alexia or components of the Gerstmann
syndrome may be associated
severe left-sided visual neglect results from a lesion
in the right angular gyrus
Visual Disorientation andDisord ers of
Spatial (Topographic)
Localization
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Patients with this disorder are unable to orient
themselves in an abstract spatial setting
(topographagnosia)
such patients have lost topographic memory
almost invariably caused by lesions in the dorsal
convexity of the right parietal lobe.
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I. Effects of unilateral disease of the parietal lobe, right or
left
A. Corticosensory syndrome and sensory extinction (or total
hemianesthesia with large acute lesions of white
matter)
B. Mild hemiparesis (variable), unilateral muscular atrophy
in children, hypotonia, poverty of movement, hemiataxia
(all seen only occasionally)
C. Homonymous hemianopia or inferior quadrantanopia
(incongruent or congruent) or visual inattention
D. Abolition of optokinetic nystagmus with target moving
toward side of the lesion
E. Neglect of the opposite side of external space (far more
prominent with lesions of the right parietal lobe—see
below)
II. Effects of unilateral disease of the dominant (left) parietal
lobe (in right-handed and most left-handed patients)—additional
phenomena include
A. Disorders of language (especially alexia)
B. Gerstmann syndrome (dysgraphia, dyscalculia, finger
agnosia, right-left confusion)
C. Tactile agnosia (bimanual astereognosis)
D. Bilateral ideomotor and ideational apraxia (
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III. Effects of unilateral disease of the nondominant (right) parietal
lobe
A. Visuospatial disorders
B. Topographic memory loss
C. Anosognosia, dressing and constructional apraxias
(these disorders may occur with lesions of either hemisphere
but one observed more frequently and are of
greater severity with lesions of the nondominant one)
D. Confusion
E. Tendency to keep the eyes closed, resist lid opening,
and blepharospasm
IV. Effects of bilateral disease of the parietal lobes
A. Visual spatial imperception, spatial disorientation, and
complete or partial Balint syndrome (optic apraxia, described
SYNDROMES CAUSED BY
LESIONS OF THE OCCIPITAL
LOBES
Visual Field Defects
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homonymous hemianopia
A lesion confined to the pole of the occipital lobe
results in a central hemianopic defect that splits the
macula and leaves the peripheral fields intact
Bilateral lesions of the occipital poles, as in
embolism of the posterior cerebral arteries, result in
bilateral central hemianopias
optokinetic responses are usually spared in
Cortical Blindness
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bilateral lesions of the occipital lobes (destruction of area
17 of both hemispheres), there is a loss of sight and a loss
of reflex closure of the eyelids to a bright light or threat
The pupillary light reflexes are preserved,
The eyes are still able to move through a full range
optokinetic nystagmus cannot be elicited
Visual imagination and visual imagery in dreams are
preserve
There may also be visual hallucinations of either elementary
or complex type
Central vision is intact
Visual Anosognosia (Anton
Syndrome
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The main characteristic of this disorder is the denial
of blindness by a patient who obviously cannot see
The lesions in cases of negation of blindness extend
beyond the striate cortex to involve the visual
association areas.
Visual Illusions (Metamorphopsias
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deformation of the image, change in size, illusion of
movement, or a combination of all three
lesions confined to the occipital lobes but are more
frequently due to shared occipitoparietal or
occipitotemporal lesions;
right hemisphere appears to be involved more often
than the left
Visual field defects are present in many of the
cases.
Visual Hallucinations
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elementary or complex, and both types have
sensory as well as cognitive aspects
They are indicative of lesions in the visual
association areas or their connections with the
temporal lobes.
The patient may realize that the hallucinations are
false experiences or may be convinced of their
reality.
Often they are associated with a homonymous
hemianopia
Visual Object Agnosia
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consists of a failure to name and indicate the use of a
seen object by spoken or written word or by gesture.
Visual acuity is intact, the mind is clear, and the patient
is not aphasic— conditions requisite for the diagnosis of
agnosia
If the object is palpated, it is recognized at once, and it
can also be identified by smell or sound if it has an
odor or makes a noise.
visual object agnosia is usually associated with visual
verbal agnosia (alexia) and homonymous hemianopia
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Prosopagnosia (the inability to identify faces; see
further on) is also present in most cases
The underlying lesions are usually bilateral
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I. Effects of unilateral disease, either right or left
A. Contralateral (congruent) homonymous hemianopia,
which may be central (splitting the macula) or peripheral;
also homonymous hemiachromatopsia
B. Elementary (unformed) hallucinations—usually due to
irritative lesions
II. Effects of left occipital disease
A. Right homonymous hemianopia
B. If deep white matter or splenium of corpus callosum is
involved, alexia and color-naming defect
C. Visual object agnosia
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III. Effects of right occipital disease
A. Left homonymous hemianopia
B. With more extensive lesions, visual illusions (metamorphopsias)
and hallucinations (more frequent with rightsided
than left-sided lesions)
C. Loss of topographic memory and visual orientation
IV. Bilateral occipital disease
A. Cortical blindness (pupils reactive)
B. Anton syndrome (visual anosognosia, denial of cortical
blindness)
C. Loss of perception of color (achromatopsia)
D. Prosopagnosia (temporo-occipital), simultanagnosia
(parieto-occipital)
E. Balint syndrome (parieto-occipital)