Altitudinal Hemianopia Caused by
Occipital Infarctions
Clinical and Computerized Tomographic Correlations
Richard P. Newman, MD; William R. Kinkel, MD; Lawrence Jacobs, MD

patients with altitudinal homonhemianopia caused by bilateral
occipital infarctions were studied. Their
clinical-computerized tomographic correlations showed the anatomic representation of the superior and inferior visual
\s=b\ Two

ymous

fields in the lower and upper banks of the
calcarine fissure, respectively. The patient with the superior-field defect was
unusual because he retained normal color
vision and facial recognition abilities,
despite having bilateral lesions that have
classically produced central achromatopsia and prosopagnosia.
(Arch Neurol 1984;41:413-418)

Altitudinal hemianopia caused by
occipital infarctions is extremely
rare. Only two cases have been re¬
ported with necropsy, both of which

had inferior altitudinal visual field
defects that appeared to have been
caused by infarctions of the upper
striate cortex; however, both cases
had involvement of infracalcarine
parenchyma as well.1·2 We report two
additional cases of altitudinal hemia¬
nopia, one involving the inferior field
Accepted for publication June 16, 1983.
From the Dent Neurologic Institute (Drs Newman, Kinkel, and Jacobs) and Departments of
Anatomy (Dr Kinkel) and Physiology (Dr
Jacobs), Division of Neurobiology, State University of New York School of Medicine, Buffalo.
Presented in part at the 33rd Annual Meeting
of the American Academy of Neurology, Toronto,
May 1, 1982.
Reprint requests to Dent Neurologic Institute,
Millard Fillmore Hospital, 3 Gates Circle, Buffalo, NY 14209 (Dr Newman).

and one involving the superior field,
caused by occipital infarctions. The

clinical-computerized tomographic
(CT) correlations showed the anatom¬
ic separation of the altitudinal fields
in the occipital lobes. The patient with
the superior-field defect also showed

that, contrary to current concepts of
central achromatopsia and prosopag¬
nosia,3·4 color vision and facial recog¬
nition ability may sometimes remain
intact, despite bilateral ventromesial

occipitotemporal damage.

REPORT OF CASES
Case 1.—A 66-year-old woman with
Guillian-Barré syndrome suffered a hyp¬
oxic episode that resulted in cortical blind¬

(left eye, no light perception; right
light perception only and normal
pupillary reactions to light). There was
gradual improvement during the next sev¬
en days, during which vision returned in
the superior field, where she could perceive
light, color, and objects.
Visual field testing showed a complete
macula-splitting, inferior altitudinal hom¬
onymous hemianopia (Fig 1, top). In the
superior field, color was perceived normal¬
ly, but perception of form was defective.
The patient was able to identify and count
fingers and recognize faces and a variety of
other objects in the superior field, but they
seemed blurred, displaced downward, and
smaller than normal (approximately one
half of normal size). On other occasions,
objects in view seemed larger than they
really were. She had difficulty reading
because of "blurriness losing place" and
also had difficulty judging distances (ob¬
jects seemed farther away than they actu¬
ally were). The patient made frequent
ness

eye,

errors in

judging which of the examiner's

two index fingers was farther away when
they were held at different distances in

front of her. She made similar errors in
estimating her distance from various
objects when looking around her room or
down the hall. She bumped into walls and
furniture as she walked down the hall. The
patient stated that she saw the objects but
did not realize they were in her way, ie, she
misjudged their positions.
Perception of sizes and shapes was also
inaccurate. When shown a square block
and instructed to outline its shape, the
patient indicated a rectangle with horizon¬
tal components approximately twice as
long as they really were. A comb, 12.7 cm in
length and held 25.4 cm in front of her,
appeared to be 38.1 cm long and approxi¬
mately 50.8 cm away from her.
No optokinetic responses could be elici¬
ted. The flight of colors5 was absent in the
right eye, and only green was seen in the
left eye. Eye movements (studied by serial
bedside observation and electro-oculography) were normal in the horizontal plane
and the upward direction; downward pur¬
suits were interrupted by saccades and
often did not follow the target through its
full range of downward motion. Flashes of
light alternately presented in the superior
and inferior fields induced normal upward
but not downward saccades. Usually, the
eyes were directed upward to the position
where the flash in the superior field had
been presented after it had been extin¬
guished and a new flash had been pre¬
sented in the inferior field. Auditory cues
that the light had flashed in the inferior
field resulted in irregular downward
searching movements. Still, the patient
could move her eyes upward and downward
normally on command when no targets
were presented. Visual evoked response

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Fig 1.—Case 1. Top, Visual fields showing superior-field altitudinal defect for form
(color perception preserved) and macula-splitting inferior-field altitudinal hemiano¬
pia, in which patient was blind. Test objects were 6-, 12-, and 15-mm red and
white targets. OS indicates left eye, and OD, right eye (tangent field). Bottom
left, Horizontal computerized tomogram (CT) showing bilateral cuneus (Cu)
infarct that spared lingual gyri (LG). Inferior calcarine (Ca) lips were also
spared, but superior Ca lips may have been involved. (Cu and superior Ca lips
were not separable by CT.) In most dorsal sections (7 and 8), precuneus re¬
gions were involved bilaterally. Levels scanned: 1-8, ventral to dorsal. Bot¬
tom right, Sagittal reconstruction of same CT. Infarct (arrowheads) involved Cu
but not LG. Sections scanned: 1-2, medial to lateral of right hemisphere. Sagit¬
tal reconstruction of left hemisphere showed essentially identical regions
of infarcted and spared parenchyma. V indicates right lateral ventricle.

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Fig 2.—Case 2. Top, Visual fields showing
superior altitudinal macula-sparing monochromatism. Form perception was absent but
motion was perceived normally. Test objects
were 1-, 6-, and 15-mm red and white targets
(tangent field). Identical field defects were
shown by automated perimetry using 4-, 16-,
and 64-sq mm targets at 1,000 apostilbs
intensity. OS indicates left eye, and OD, right
eye. Bottom left, Horizontal computerized
tomogram (CT) showing infarcts of lingual
(LG), occipitotemporal (OT), and parahippocampal (PH) gyri bilaterally, with some
involvement of inferior lip of calcarine cortex
(Ca) on right. Upper lips of Ca (arrowheads)
appeared to be spared bilaterally. Levels
scanned: 1-6, ventral to dorsal. Bottom
right, Coronal reconstruction of same CT.
Infarcts (arrows) were located inferolaterally to occipital horns and extended posteromedially to involve occipital poles (1 and 2).
Left-sided lesion extended farther anteriorly
into PH gyrus than that on right. Glomeruli of
choroid plexus within occipital horns of ven¬
tricles is visible (4), as is third ventricle in
midiine (3 and 4). Sections scanned: 1-4,
posterior to anterior.

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(VER) testing (black and white checker¬
board; full-field and separate altitudinal

superior- and inferior-field stimulations)
showed that cortex-dependent responses
were present but so poorly developed that
further interpretation was not possible.
The patient had amblyopia in the right
eye, first identified in early childhood, and

had worn corrective lenses ever since.
Visual acuity at the time of this examina¬
tion was 20/800 OD and 20/30 OS (un¬
changed from measurements taken during
the previous 15 years). There were mild
cataract formations bilaterally. Mental
status was normal.

The CT showed bilateral, nearly sym¬
metric infarctions of the occipital lobes in
the territories of the parieto-occipital
branches of the posterior cerebral arteries
(Fig 1, bottom left). The narrow bands of
the infarct involved parenchyma posterior
and superior to the calcarine fissures but
not inferior to them. Their most medial
extent was to the midiine; laterally, they
extended to the area of the parieto-occipi¬
tal sulci. The lesions were directly confined
to the cunei from the level of the quadrig¬
eminal cistern ventrally to the supraventricular level dorsally. Near the convexi¬
ties, the lesions extended into the precuneate gyri bilaterally. The inferior calcarine
lips appeared to be spared, but the upper
calcarine cortices may have been involved,
as it was impossible to identify them sepa¬
rately from the infarcted cunei. Sagittal
reconstruction showed sparing of lingual
gyri and the dorsal extent of the lesions
into the precuneate regions bilaterally (Fig
1, bottom right).
Case 2.—A 57-year-old man had episodes
(lasting seconds to minutes) during which
time he saw "white lights" moving from
left to right without obscuring vision.
These episodes had recurred numerous
times for four years. Seven months prior to
our examination, the frequency and inten¬
sity of the episodes increased, and the
position of the lights changed so that they
occupied the superior altitudinal portion of
his visual field, where they took on "geo¬
metric" designs, such as "prisms" and
"diamonds," still moving from left to right.
The patient suddenly began to miss traffic
signals while driving and could not see his
hair or forehead when looking in a mirror.
At this time, the geometric designs disap¬
peared. He complained that visual objects
viewed in the superior portions of the
visual field appeared "whitish" and "spon¬

gy-"

A variety of objects (eg, pictures, bills,
coins, books, and clothing) presented in the

patient's superior visual field could not be
seen because they were obscured by a
"washed-out, spongy" appearance. When
the objects were moved, he could perceive
the motion but was unable to identify the
moving object, ie, its size, shape, texture,
or

color, until it was moved into the inferi¬

field.
Vision in the inferior field (including
color perception) was completely normal.
The patient had no difficulty recognizing
faces as long as he could use the inferior
field, at least partially. When he looked at
or

the examiner's face (or his own in a mir¬
ror) and fixated the nose without moving
his head to use the inferior field, the
forehead appeared "spongy" and "washed
out"; the hair could not be seen. The
patient adjusted for this by slight exten¬
sion of his neck, facilitating vision with the
inferior field. Flashes of light and other

stationary targets presented to his superi¬
or field induced searching movements and
failure to arrive on target. However, mov¬
ing targets (eg, wiggling fingers) presented
in the superior field induced normal
upward saccades that were on target.
Upward pursuits were normal as long as
the targets were initially fixated in the
inferior field. Otherwise, eye movements
were normal.

Visual field testing revealed complete,

congruous, macula-sparing (2° to 3°) supe¬

rior altitudinal homonymous hemianopia,
where motion was perceived but form and
color were not (Fig 2, top). Color perception
(shown by a variety of objects tested in
bright and dim illumination) was normal
in the inferior field, as were Ishihara's
design charts and pseudoisochromatic
plate interpretations. Hue discrimination
(similarity ordering of 12 variations of the
four primary colors)6 was normal in the
inferior field. The patient could name from
recollection the colors of a variety of com¬
mon objects (eg, lemon and fire engine).
Reading was normal in the inferior field;
so was writing. There was no dysnomia or
other evidence of dysphasia. Mental status
was normal. Visual acuity was 20/25 in the
right eye, and 20/30 in the left eye, with
corrective lenses. For five years following
ictus, the patient reported being able to see
some objects in the peripheral temporal
portions of the superior fields, especially in
bright light. However, serial visual field
tests failed to show any change from the

original tests.

The CT showed bilateral areas of infarc¬
tion involving the lingual, occipitotemporal, and parahippocampal gyri (Fig 2, bot¬
tom left) in the territories of the posterior
temporal branches of the posterior cere¬
bral arteries. The infarctions appeared to
destroy totally the lingual gyri bilaterally.
The medial aspects of the occipitotemporal
(fusiform) gyri were also involved symmet¬
rically. The parahippocampal gyri were
involved bilaterally, but asymmetrically,
the left-sided infarction extended further
anteriorly than that on the right. There
was a wedge-shaped infarct of the striate
cortex on the right side only. The hippo¬
campal, cunéate, and lateral occipital gyri
were spared. Preserved parenchyma of the
medial and lateral occipital pole regions
(Fig 2, bottom left, section 3) appeared to
be composed of lateral occipital gyri and
posterior caudal extents of cunei bilateral¬
ly. The only tissues that appeared to be
preserved at the anteromedial aspects of
the lingual infarct were those of the tento¬
rium. Coronal reconstruction showed the
ventrodorsal and anteroposterior extents
of the lesions, from ventrolateral to occipi¬
tal horns of the lateral ventricles to the
occipital pole bilaterally (Fig 2, bottom

right).

COMMENT

Although some authors have sug¬
gested that altitudinal hemianopia is
usually a manifestation of a chias¬
matic or prechiasmatic lesion,7"' Bend¬

er10 found that this visual field defect
is most commonly caused by bilateral
occipital lesions, as seen in our
patients. Still, the rarity with which
occipital lesions produce such field
defects is attested to by the fact that
there were only five patients with
altitudinal hemianopia in the com¬
bined series of Holmes and Lister,11
Holmes,12 Teuber et al,13 and Money
and Nelson.14 All of these authors
noted inferior altitudinal defects pre¬
sumably caused by bilateral lesions
above the calcarine fissure, though
the location of the responsible lesions

(upper posterior optic radiations) was

confirmed by necropsy in only one
case.12 No superior-field altitudinal
defects were encountered in patients
with trauma, probably because the
occipital parenchyma that would have
had to be involved to produce that
field defect (inferior to the calcarine
fissure) lie adjacent to large venous
structures (eg, the straight sinus) and
penetrating wounds in that region
would have been likely to cause fatal

hemorrhage.

While the vascular supply of the
occipital lobes has been described in
detail15 and a variety of visual defects
resulting from discrete occlusions
have been reported, there have been,
to our knowledge, only two patients
with altitudinal hemianopia due to
vascular lesions of the occipital lobes
who have undergone autopsy.1·2 Both
patients had complete altitudinal
hemianopia of the inferior visual
field, combined with some impair¬
ment of the superior field. Their
defects were attributed to bilateral
infarcts of the occipital parenchyma
above the calcarine fissure, but nei¬
ther case was pathologically "clean,"
as both had some involvement of the
infracalcarine parenchyma as well.
The method of CT provides an excel¬
lent opportunity to correlate visual
defects with occipital vascular lesions.
The CT patterns of abnormalities that
correspond to different branch occlu¬
sions of the posterior cerebral arteries
are known.16 In addition, the scans are
performed during life, when immedi¬
ate correlations with visual defects
can be performed and serial scans can
be compared with changes in visual
defects. However, to the best of our
knowledge, there have only been two
CT reports (of four cases of vascular
lesions) correlating altitudinal hom-

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hemianopia with occipital
lesions.17·18 The CT information pro¬
vided in both reports was insufficient
to make more than a general correla¬
tion between the occipital anatomy
involved and the visual field defects
produced. A patient with incongruous
onymous

superior altitudinal hemianopia, cen¬
tral achromatopsia, and prosopagno¬

sia had bilateral lesions of the "inferoposterior aspects of the cerebral
cortex extending anteriorly into the
temporal lobe and posteriorly to the

occipital pole."17
Only one CT section (showing the
ventral aspect of a left-sided lesion)
was published; other sections were
reported to show an infarct in similar
inferior regions on the right. Judging
from this limited information, the
infarcts may have involved the lin¬

gual, occipitotemporal, parahippo¬
campal, and, possibly, inferior tempo¬
ral gyri, but this could not be deter¬
mined with certainty. The anatomic
correlations of three other patients
with altitudinal homonymous hemia¬
nopia (one in the superior field, two in
the inferior field) were limited to the
levels of CT sections (relative to the
pineal body) where the occipital

lesions were best visualized. No other
anatomic information on these pa¬
tients was provided.18
Our patients' clinical-CT correla¬
tions clearly showed the representa¬
tion of altitudinal visual fields in the
occipital lobes above and below the
calcarine fissures. In patient 1, the
infarcts in the distribution of parieto¬
occipital branches of the posterior
cerebral arteries produced discrete
involvement of the cunei bilaterally.
This finding confirmed results of pre¬
vious necropsy studies that correlated
inferior altitudinal hemianopia with
bilateral lesions above the calcarine
fissures. The macular-splitting nature

of this patient's hemianopia sug¬
gested that the upper striate cortex
(calcarine branches) was also involved
bilaterally. However, this could not be
shown with certainty because the

upper parts of striate cortices could
not be distinguished from the inferior

aspects of infarcted cunei with cur¬

rently available CT techniques. Vision
was normal in patient l's preserved
homonymous superior field (return of
premorbid acuity; light and color per¬
ception), except for defective form
perception, which we attributed to the
dorsal extension of her lesion into the
parietal lobes. There was no CT evi¬
dence for involvement in the region of
the inferior calcarine cortex or infra¬
calcarine parenchyma.
Patient 2's infarcts in the distribu-

tion of the calcarine branch on the
right and of posterior temporal
branches of the posterior cerebral
arteries bilaterally clearly showed
that bilateral lesions inferior to cal¬
carine fissures caused superior altitu¬
dinal hemianopia. The lesions ap¬
peared to destroy completely the lin¬
gual gyri bilaterally and involved
large portions of the occipitotemporal
and parahippocampal gyri bilaterally
(on the left more than on the right).
The congruous macular-sparing na¬
ture of the patient's hemianopia led us
to postulate that the involvement of
the right inferior striate cortex was
incomplete, but confirmation of this
postulate was beyond the resolution of
CT.
The visuopsychic phenomena asso¬
ciated with the field defects of these
patients deserve comment. Patient 1
experienced cortical blindness that
persisted for seven days before resolv¬
ing into a permanent altitudinal infe¬
rior-field defect. This defect has been
accompanied by a behavioral abnor¬
mality best classified as visual disori¬
entation,19 which also appeared to be
permanent (present for four years
since ictus). The errors in absolute
and relative localization of objects in
space;

difficulty avoiding objects

when walking and finding her way
about; defective stereopsis (including
teleopsia), sometimes with micropsia,
other times with macropsia; and trou¬
ble reading are components of visual
disorientation with metamorphopsia
that might be expected, in view of the
dorsal extension of her lesions into
the precuneus regions. The phenome¬
non of visual disorientation has clas¬
sically been associated with such
bilateral parietal lesions.19
Patient 2 is noteworthy because of
the absence of permanent visuopsyc¬
hic abnormalities, despite lesions that
should have produced two such defi¬
cits. He experienced occipital irrita¬
tive phenomena in the form of moving
photisms, which ceased when his
superior-field defect appeared. No
other visuopsychic disorder has devel¬
oped during five years of follow-up
since ictus. The patient has retained
normal color vision in the inferior
visual field, and his ability to recog¬
nize faces has been unaffected, despite
the presence of bilateral lesions that
characteristically produce central
achromatopsia and prosopagnosia.
There is a body of evidence, includ¬
ing four autopsy cases,2023 and CT
analysis of two cases of central achro¬
matopsia,3 that indicates that the
total cortical representation of color
perception from one homonymous

visual field is contained in the contralateral lingual and occipitotemporal
gyri (analagous to area V4 of the
macaque).24·25 A review of available
literature indicated that when lingual
and occipitotemporal lesions are
bilateral, prosopagnosia can result

(usually accompanied by achromatop¬
sia).4 The ten autopsies and three CTexamined patients with prosopagno¬

sia had bilateral lesions of these mesi¬
al occipitotemporal regions (some¬
times extending into the parahippo¬
campal and inferior temporal gyri).4
Why our patient 2 retained normal
color vision and facial recognition
abilities is unknown. The lingual gyri
appeared to be completely destroyed
bilaterally. Both occipitotemporal and
parahippocampal gyri were also
extensively involved, but the lesions
were asymmetric, with that on the
left extending farther anteriorly than
that on the right. Possibly, the pre¬
served anterior portion of the right
parahippocampal gyrus was critical
for retention of color vision, despite
the presence of bilateral lesions. The
relative superiority of the right over
the left hemisphere in the process of
facial recognition has recently been
stressed in a study of patients with a
surgically split corpus callosum.26
Most of the preserved parenchyma at
the occipital poles appeared to be
those of lateral occipital gyri. Con¬
ceivably, those gyri, combined with
the preserved right parahippocampal
gyrus, were sufficient for retention of
color vision and facial recognition
abilities. However, the lateral occipi¬
tal gyri have not been implicated pre¬
viously as important structures for
these abilities.
Previous reports of normal VERs in
blind persons attributed the pre¬
served potentials to intact striate cor¬
tices when association areas were
destroyed,27 or to preserved associa¬
tion areas when striate cortices were
destroyed.28 It is possible that both the
striate cortex and association areas
must be involved before occipital
lesions will cause a loss of VER. Thus,
the VER findings in our patients (case

1, nearly absent; case 2, normal)
might be explained by involvement of

the striate cortex and visual associa¬
tion areas in patient 1, but only visual
association areas in patient 2. The
nearly absent VER of patient 1 might
also have been related to her limited
ability to recognize and be attentive to
the checkerboard pattern on the
screen, because of visual disorienta¬
tion.
The nearly absent flight of colors in
case 1 may have been due to bilateral

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supracalcarine and infracalcarine in¬
volvement caused by the patient's ini¬
tial hypoxic episode, although only the
supracalcarine lesions were visible by
CT. The normal flight of colors in

case 2 showed the intactness of cere¬

bral structures that generate colorful
afterimages.5 Their absence was
expected in this patient's hemianopic
superior field, where all perception

except that of motion had been lost.

This research was supported by grants from
the Dent Family Foundation and Delaware

North Companies, Buffalo.
Antonio R. Damasio, MD, gave helpful advice
in the preparation of this article.

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