The Representation of the Visual
Field in Human Striate Cortex
A Revision of the Classic Holmes
Jonathan C. Horton, MD, PhD, William F.
\s=b\ We have tested the
accuracy of Gor-
don Holmes' retinotopic map of human
striate cortex by correlating magnetic
resonance scans with homonymous field
defects in patients with clearly defined
occipital lobe lesions. Our findings indi-
cate that Holmes underestimated the cor-
tical magnification of central vision. In a
revised map of the human striate cortex,
we expand the area subserving central
vision and reduce the area devoted to
peripheral vision. These changes bring
the map of human striate cortex into
agreement with data reported for closely
related nonhuman primate species.
(Arch Ophthalmol. 1991;109:816-824)
"1 he representation of the visual field
in the human striate cortex was
originally studied by Inouye,1 an oph¬
thalmologist who treated wounded
survivors of the 1904-1905 Russo-Japa¬
nese War.1,2 He correlated visual field
deficits with the trajectory of missiles
penetrating the occiput to construct
the first retinotopic map of the striate
cortex. A decade later, Holmes and
Lister3 examined soldiers injured in
World War I and confirmed the essen¬
tial features of Inouye's map.3J The
familiar Holmes map (Fig 1) has been
widely reproduced in textbooks and
still provides the most detailed source
of primary data concerning the repre¬
sentation of the visual field in the
human striate cortex. '
Accepted for publication December 26, 1990.
From the Neuro-ophthalmology Unit, Depart-
ments of Ophthalmology, Neurology, and Neuro-
surgery, University of California, San Francisco.
Reprint requests to Neuro-ophthalmology
Unit, U-125, University of California San Francis-
co, San Francisco, CA 94143-0350 (Dr Horton).
Map
Hoyt, MD
The Holmes map depicts an orderly,
topographic representation of the con¬
tralateral hemifield of vision in the
striate cortex. The vertical meridian is
represented along the perimeter of the
striate cortex. The representation of
the horizontal meridian runs along the
base of the calcarme fissure. The mac¬
ula occupies the occipital pole, while
the periphery of the visual field is
mapped anteriorly. Both Inouye and
Holmes realized that the central reti¬
na, more densely cellular and special¬
ized for best visual acuity, has a rela¬
tively expanded representation in the
striate cortex. Using a planimeter, we
have examined the maps of the striate
cortex published by Inouye and
Holmes to calculate the area appor¬
tioned to central vision. Our analysis
indicates that both investigators as¬
signed 25% of the surface area of stri¬
ate cortex to the central 15° of vision.
After the introduction of computed
tomography, the accuracy of the
Holmes map was confirmed by clinico-
radiologie correlation. In a series of
pioneering studies, occipital lesions
were localized by computed tomogra¬
phy in patients with visual field defi¬
cits.""9 A good match was reported be¬
tween the neuroradiological findings
and the location of lesions predicted by
the Holmes map. However, these ear¬
ly studies were limited by the rather
poor resolution of early computed
tomography.
The striate cortex has been carefully
mapped using modern electrophysio-
logic methods in a number of Old
World primate genera: Papio, Cerco-
pithecus, and Macaca.10'1" These re-
ports have shown that central vision
occupies an enormous fraction of the
striate cortex in Old World primates.
For example, in macaque monkeys,
the central 15° of vision fills about 70%
of the total surface area of the striate
cortex.1112 This figure far exceeds the
proportion (25%) allotted by Holmes
and Inouye to the central 15° in human
striate cortex.
The discrepancy between the human
and monkey data suggests either that
the Holmes map requires modification
or that human visual cortex is funda¬
mentally different from monkey visual
cortex in terms of the percentage of
striate cortex devoted to central vi¬
sion. Over the past year, we have
correlated magnetic resonance images
with visual field deficits in our patients
with occipital lobe lesions to help us
decide between these two alternatives.
In this report, three typical cases are
analyzed in detail to illustrate the clini¬
cal evidence we have collected to sup¬
port amendment of the Holmes map.
REPORT OF CASES
CASE 1.—A 30-year-old woman from In¬
dia reported several brief episodes of flash¬
ing, colored lights in her right upper quad¬
rant of vision. The visual acuity in each eye
was 20/20 without correction. She denied a
visual field deficit, but testing at the tan¬
gent screen showed a zonal scotoma in the
right upper quadrant from 6° to 18° (Fig 2,
inset). In the right eye the scotoma was
contiguous with the blind spot. Within the
scotoma, the patient could not see a 15-mm
or 30-mm white disk at a distance of 2 m,
except along a fringe near the vertical
meridian. In this relative portion of the
scotoma, she could detect a 15-mm white
disk but not a 5-mm white pin. The visual
 field defect was also documented by map¬
ping thresholds from 0° to 60° with a Hum¬
phrey Field Analyzer (Allergan-Humphrey
Instruments, San Leandro, Calif) (Fig 2).
A ,-weighted magnetic resonance scan
showed a sharply delineated lesion in the
left occipital lobe, abutting the tentorium
(Fig 3). The relationship of the lesion to the
approximate boundaries of the striate cor¬
tex is shown schematically (Fig 3, right).
The patient's occipital lobe measured 56 mm
from the occipital pole to the confluence of
the calcarme and parieto-occipital sulci
(where the striate cortex ends rostrally).
The lesion began 22 mm from the occipital
pole and extended anteriorly for 14 mm.
At craniotomy, a nodule filled with puru¬
lent material was excised. Specimens for
bacteria, fungus, and mycobacteria were
negative. Microscopic examination showed
a necrotizing granuloma consistent with a
presumed tuberculoma. The patient is im¬
proving on a regimen of isoniazid, rifampin,
and ethambutol.
CASE 2.—A 28-year-old woman recount¬
ed a history of migraine that began when
she was a high school student. Typical
attacks started with shimmering silver lines
in the left visual field, followed by a left
homonymous hemianopia, headache, and
nausea. A computed tomographic scan was
obtained when the left homonymous hem¬
ianopia persisted after an unusually severe
migraine attack. It revealed a right occipi¬
tal lobe arteriovenous malformation that
was confirmed by cerebral arteriography.
When the patient was examined 5 months
later, the visual acuity was 20/20 in each Fig 1 .—The Holmes5 map (1945) showing the representation of the visual field in the human
eye. Tangent screen testing at 2 m showed striate cortex (primary visual cortex, V1 ). The map underestimates the relative magnification of
a left homonymous heminanopia to 30- and central vision. For example, the 30° ¡soeccentricity contour (arrow) in the Holmes map is
5-mm white targets (Fig 4). The field defect
intersected the upper vertical meridian at
represented where the 12° ¡soeccentricity contour is actually located. (From Holmes5.)
10°, crossed the horizontal meridian at 15°
(through the left eye's blind spot), and 1.5° could be mapped along the upper verti¬
intersected the lower vertical meridian at tion: it extended from 6° to 18° and was
20°. The visual field thresholds were also cal meridian and the lower vertical merid¬ centered at an eccentricity of 12°. In
plotted with the Humphrey Field Analyzer ian. The extent of macular sparing varied
from 0.5° to 4.0°. The I2e and III4e isopters
the second patient, the Holmes map
(Fig 4). were identical when plotted with a Gold- predicts a field cut between 40° and
A magnetic resonance image obtained
mann perimeter (Fig 6). The visual field 90°. However, visual field testing
before surgery showed a lesion replacing
the anterior portion of the right calcarme defects in the right eye and left eye were showed a scotoma that approached
cortex (Fig 5). It began 31 mm from the congruous. within about 15° of fixation. Finally, in
A magnetic resonance scan showed bilat¬ the third patient, the cortical infarcts
occipital tip and extended rostrally 33 mm eral infarcts involving visual cortex along
to terminate at the parieto-occipital sulcus. should have resulted in sparing of the
The lesion was excised successfully. the medial surface of the occipital lobe (Fig central 15° of vision in each hemifiekl
CASE 3.—A 57-year-old woman awoke 7). The posterior 10 mm of cortex along the
interhemispheric fissure appeared spared according to Holmes. Instead, we
with a headache and noticed some difficulty found bilateral macular sparing that
with her peripheral vision on the left side. on each side. In addition, the occipital poles
and opercula were intact bilaterally (Fig 7, reached a maximum of only 4°.
She gashed the left side of her forehead on In all three patients, the Holmes
an open cupboard door while preparing right).
breakfast. A week later, after rinsing her The patient was retested 2 months after map correlates poorly with the actual
face in a bathroom sink, she suddenly be¬ her stroke. Her visual fields were location of the lesion imaged by mag¬
came completely blind. She was admitted to unchanged. netic resonance, even if one allows for
the hospital where a small island of central COMMENT natural variation in the exact dimen¬
vision gradually returned over the next few sions and location of the striate cortex
days. The visual field deficits in our pa¬ that occurs from patient to patient.
When the patient was examined, the tients are incompatible with the Collectively these cases demonstrate
visual acuity was 20/20 in each eye without Holmes map of the striate cortex.5 that central vision occupies a greater
correction. The patient was positioned ex¬
actly 57 in from the tangent screen for According to his map, in the first pa¬ proportion of the human striate cortex
tient the tuberculoma should have than Holmes portrayed in his retinoto¬
visual field testing. At this distance, 1 in on
the tangent screen equals 1° of visual field. caused a scotoma between 20° and 40°, pic map. In 1952, Spalding" published
Examination showed bilateral homonymous centered at an eccentricity of about 30° a revision of the Holmes map based on
hemianopia with macular sparing in both (Fig 1, arrow). In fact, the patient's clinical findings in wounded veterans
hemifields (Fig 6, inset). A vertical step of scotoma was smaller and closer to fixa- of World War II. Although the Spai-
Fig 2.—Merged 30-2 and 60-2 full-threshold visual field tests performed by patient 1 using a Humphrey Field Analyzer. A
homonymous, congruous scotoma was present in the right upper quadrant using a 0.43° test spot against a background
illumination of 31.5 apostilbs. Within the scotoma, thresholds for detection of the test spot were greater than 10 000
apostilbs. Elsewhere in the visual field the thresholds were normal. Inset, Visual fields of patient 1 are mapped at the tangent
screen. The scotoma extended from 6° to 18°. 5/2000W indicates 5-mm white pin at 2000 mm; 15:30/2000W, 15- or 30-mm
white disk at 2000 mm.

Fig 3. —Parasagittal magnetic resonance image of the left occipital lobe in patient 1. The lesion in the visual cortex
produced the visual field defect shown in Fig 2. Scale 5 cm. Right, Note location of the lesion (cross-hatched area) relative
=

to the likely extent of striate cortex (stippled area). The striate cortex exposed on the lateral surface of the hemisphere is not
seen in this sagittal view. The calcarine sulcus (solid arrow) and the parieto-occipital sulcus (open arrow) are marked by
dots. These sulci were better visualized on parasagittal images closer to midline.
 Fig 4. —Full-threshold 60° visual fields in patient 2 mapped using a Humphrey Field Analyzer. The central 15° of the left
hemifield were intact. The visual field of the left eye was tested with the blind spot monitor off (otherwise the instrument
attempts futilely to plot the blind spot). Inset, Tangent screen plot of visual fields shows that the field defect actually bisects
the blind spot representation of the left eye. 30:15/2000W indicates 15- or 30-mm white disk at 2000 mm.

ding map assigns slightly more cortex

to central vision than the Holmes map,
it still fails to allocate sufficient cortex
to the representation of central vision.
Daniel and Whitteridge" published
the first complete map of macaque
striate cortex based on microelectrode
recordings. They invented the term
linear magnification factor to refer to
the millimeters of cortex representing
1° of visual field at any given eccentric¬
ity. Their data showed a ratio of more
than 40:1 in linear magnification factor
between the fovea (0° eccentricity) and
periphery (60° eccentricity). The areal
magnification factor millimeters
squared of cortex/degree squared—has
—

a ratio of more than 1000:1 between

the fovea and 60°. Van Essen and
colleagues12 have also studied the rep¬
resentation of the visual field in the
macaque striate cortex. Their map is in
close agreement with the findings re¬
ported by Daniel and Whitteridge. Be¬
tween 55% and 60% of the surface area
of the striate cortex is occupied by the
representation of the central 10° of
vision.
Fig 5. ,-weighted parasagittal magnetic resonance image through the right occipital lobe in
patient 2 shows the arteriovenous malformation responsible for the visual field defect illustrated
—

A Revised Map of the

in Fig 4. The posterior margin of the lesion is situated 31 mm from the occipital tip, marking the Human Striate Cortex
approximate location of the representation of the left eye's blind spot (eccentricity 15°). The
=

calcarine (curved arrow) and parieto-occipital (straight arrow) sulci are indicated. Scale 5 cm.
= The findings in our patients suggest
(From Holmes.5) that the relative magnification of cen-
 Fig 6.—Visual fields of patient 3 plotted using a Goldmann perimeter show bilateral homonymous hemianopia with bilateral
macular sparing. In the right hemifield, the macular sparing is slightly greater. Because the visual field defects (right and left
eyes) were perfectly congruous, they are drawn on a single field chart. Inset, Magnified plot of residual visual fields of patient
3 tested at the tangent screen (note scale marker). The steps across the upper vertical meridian and the lower vertical
meridian each measured 1.5°. Macular sparing ranged between 0.5° and 4°.

trai vision in the human striate cortex
agrees more closely with the laborato¬
ry data obtained from macaque mon¬
keys than with the clinical data report¬
ed originally by Inouye and Holmes. A
revision of the Holmes map, scaled to
the cortical magnification found in the
macaque striate cortex,1112 is presented
in Fig 8. The foveal representation is
located at the occipital pole, where the
striate cortex usually extends about 1
cm onto the lateral convexity of the
occipital lobe (operculum). The ex¬
treme periphery of the visual field is
represented anteriorly, at the junction
of the calcarine and parieto-occipital
fissures. Only a small portion of the
striate cortex, containing the repre-
sentation of the vertical meridian, is
exposed on the medial surface of the
occipital lobe (Fig 8, top right). Most of
the striate cortex is actually buried
within the depth of the calcarine fis¬
sure (Fig 8, top left), making it diffi¬
cult to depict the coordinates of the
map directly on the cortical surface. A
better view of the visual field map can
be obtained by schematically unfolding
and flattening the visual cortex to arti¬
ficially create a planar surface (Fig 8,
bottom left). The striate cortex con¬
tains a topographic but highly distort¬
ed representation of the contralateral
hemifield of vision (Fig 8, bottom
right).
In artificially flattened maps of
caque monkey visual cortex, the stri¬
ate cortex appears as an ellipse ap¬
12
proximately twice as long as wide."
The average surface area of macaque
striate cortex is 1200 mm2.12 Estimates
of the total surface area of human
striate cortex range considerably, re¬
flecting natural variation from speci¬
men to specimen and technical differ¬
ences from laboratory to laboratory.
The most detailed study reports a
mean area of 2134 mm2 in formalde¬
hyde solution-fixed brains.15 Allowing
about 15% for shrinkage caused by
fixation, the average human striate
cortex measures about 2500 mm2. As¬
suming that the configurations of hu¬
ma- man and macaque striate cortex are
 Fig 7.—Axial proton density-weighted magnetic resonance image through the occipital lobes in patient 3 shows bright
signal in the calcarine cortex along the interhemispheric fissure that represents a recent infarct. Scale 5 cm. R indicates
=

right; P, posterior. Right, Note location of lesions (cross-hatched areas) and approximate location of striate cortex (stippled
areas). Intact striate cortex is indicated by the dashed occipital lobe border. In the left occipital lobe, about 2 cm of the striate
cortex was preserved posteriorly, accounting for 2.5° of macular sparing in the right visual hemifield.

similar, the human striate cortex is
shaped like an ellipse measuring about
80 40 mm (Fig 8, bottom left).
Our revised map (Fig 8) can be used
to localize more accurately a lesion in
the striate cortex that creates a deficit
in the visual field. Conversely, from a
magnetic resonance image of sufficient
resolution, the coordinates of a scoto¬
ma produced by a lesion in the striate
cortex can be predicted.
Figure 9, top, shows the lesion in
our first patient, inferred by plotting
the visual field deficit (Fig 2) on the
map of the human striate cortex (Fig
8, bottom left). The lesion involves 378
mm2 of tissue, or about 15% of the
mean surface area of the striate cor¬
tex. This figure was determined by
measuring directly the shaded area in
Fig 9, top, with the aid of a planime-
ter. The match between the dimen¬
sions and location of the lesion derived
from the cortical map (Fig 9, top) and
the actual dimensions and location im¬
aged by magnetic resonance (Fig 3) is
excellent.
The right visual field deficit in our
third patient is plotted in Fig 9, cen¬
ter. Planimetrie analysis indicates that
564 mm2 of tissue in the left striate
cortex remained intact after the
stroke, corresponding to 22% of the
mean striate surface area. The mag¬
netic resonance data also fits the corti¬
cal map well. The patient's scan (Fig 7)
shows sparing of 1 cm of the striate
cortex at the posterior end of the cal¬
carine fissure and sparing of another 1
cm of the striate cortex on the exposed
operculum. This magnetic resonance
image provides the first illustration of
the neuroradiologic findings in a pa¬
tient with macular sparing.
Macular Sparing
This latter case helps to dispel some
of the mystery surrounding the age-old
problem of macular sparing. Inouye1
discovered macular sparing in some of
his wounded soldiers. Therefore, in his
map he included a small representation
of the ipsilateral macula in each occipi¬
tal lobe.1 Although Holmes'' dropped
this feature from his map (Fig 1),
bilateral representation of the macula
is frequently invoked to explain macu¬
lar sparing. According to this notion,
macular vision may be preserved after
complete destruction or removal of one
occipital lobe because the macula is
dually represented in the fellow occipi¬
tal lobe. This explanation is obviously
untenable in our second patient, who
suffered bilateral occipital infarcts.
Moreover, experiments in the ma¬
caque monkey have unequivocally
ruled out any substantial bilateral rep¬
resentation of the macula in the striate
cortex.1"1316 Dow et al13 report that in
the foveal representation, no striate
receptive field centers are found more
than 5 minutes (1/12 of ) into the
ipsilateral visual field.
A nasotemporal overlap across the
vertical midline about 1° wide in the
central retina occurs in ganglion cell
projections to the brain.1'"2" This imper-
feet decussation has been advanced by
some authors as an explanation for
macular sparing.1" If correct, macular
sparing should also occur after lesions
of the optic chiasm or optic tract. How¬
ever, in the experience of most clini¬
cians, macular sparing is a cortical
phenomenon. Moreover, this theory
could account at best for only 1° to 2° of
macular sparing. In practice, macular
sparing often extends well beyond an
eccentricity of 2°.
The extremely high cortical magnifi¬
cation of the macula provides the key
to understanding the phenomenon of
macular sparing. In most patients, the
vascular supply to the striate cortex is
provided entirely by branches of the
posterior cerebral artery. Therefore, a
macula-splitting hemianopia ensues af¬
ter infarction of the posterior cerebral
artery. However, in a considerable mi¬
nority of patients, the occipital pole
straddles the vascular territories of
the posterior cerebral artery and the
middle cerebral artery.21 In these pa¬
tients, the occipital pole remains intact
after posterior cerebral artery infarc¬
tion due to perfusion by the middle
cerebral artery. Because the represen¬
tation of the central visual field is so
magnified in the caudal half of the
striate cortex, preservation of any por¬
tion of this region after posterior cere¬
bral artery occlusion will spare cortex
devoted exclusively to macular vision
(Fig 8, bottom left). Relatively large
variations in the amount of surviving
cortex from patient to patient will
Fig 8. —Revised map of the representation of the visual field in the human striate cortex. It is important to emphasize that
considerable variation occurs among individuals in the exact size and location of striate cortex. This new map provides the
best fit for our data. Top left, Note view of the left occipital lobe with the calcarine fissure opened, exposing the striate cortex.
Dashed lines indicate the coordinates of the visual field map. The representation of the horizontal meridian runs
approximately along the base of the calcarine fissure. The vertical lines mark the ¡soeccentricity contours from 2.5° to 40°.
The striate cortex wraps around the occipital pole to extend about 1 cm onto the lateral convexity, where the fovea is
represented. Top right, Note view of the left occipital lobe showing the striate cortex, which is mostly hidden within the
calcarine fissure (running between arrows). The boundary (dashed line) between the striate cortex (V1) and extrastriate
cortex (V2) contains the representation of the vertical meridian. It is usually located along the exposed medial surface of the
occipital lobe as shown, but variation occurs in specimens. Bottom left, Schematic map shows the projection of the right
visual hemifield (bottom right) on the left visual cortex, by transposing the map illustrated in the top left onto a flat surface.
The striate cortex is an ellipse about 80 40 mm, measuring roughly 2500 mm2 (40 mm 20 mm ir 2500 mm2). The row
=

of dots indicates where the striate cortex folds around the occipital pole: the small region between the dots and the foveal
representation is situated on the exposed lateral convexity of the occipital lobe. The black oval marks the region of the striate
cortex corresponding to the visual field coordinates of the contralateral eye's blind spot. This region of cortex receives visual
input only from the ipsilateral eye. HM indicates horizontal meridian. Bottom right, Right visual hemifield (of one of us
[J.C.H.]) shows the V4e isopter plotted with a Goldmann perimeter (by W.F.H.). The stippled region corresponds to the
monocular temporal crescent that is mapped within the most anterior 8% to 10% of the striate cortex (see stippled region of
map in bottom left).
 manifest clinically as modest differ¬
ences in the precise number of degrees
of macular sparing.
Our revision of the Holmes map also
helps to explain why the pattern-shift
visual evoked potential is essentially a
function of macular vision. According
to Yiannikas and Walsh,22 the central
8° generates more than 60% of the
amplitude of the evoked potential
waveform (P100). This finding has puz¬
zled clinical electrophysiologists famil¬
iar with the Holmes map. In practice,
the actual magnitude of the visual
evoked potential depends on many fac¬
tors, including the surface area of the
cortex stimulated and its orientation
with respect to the recording elec¬
trodes. Our map is in good accord, at
least qualitatively, with the observa¬
tion that stimulating beyond the cen¬
tral 10° or 15° of visual field contrib¬
utes little to the amplitude of the
visual evoked potential.
Our modification of the Holmes map
has implications for computerized visu¬
al field testing. The acquisition of
threshold data using these automated
instruments is so time-consuming that
testing is often restricted to the cen¬
tral 24° or 30° of vision. Failure to test
the visual field beyond 30° raises the
worry that some cortical lesions may
escape detection. Fortunately, the
high magnification of central vision
mitigates this danger. For example, a
30° visual field examination actually
tests the function of 83% of the striate
cortex (Fig 9, bottom). A mere 24°
field examination (which approaches
30° in the nasal hemifield when per¬
formed using a Humphrey Field Ana¬
lyzer) covers 80% of the cortical sur¬
face area.
Our amended map is also consistent
with the paucity of reported cases de¬
scribing visual field deficits confined
entirely to the monocular temporal
crescent. The temporal crescent is rep¬
resented at the rostral end of the stri¬
ate cortex. It lacks ocular dominance
columns because input is received only
from the contralateral eye.23 In human
striate cortex this region has been
identified and measured directly.24 It
constitutes less than 10% of the total
surface area of the striate cortex. The
temporal crescent representation is
compressed into a much smaller area of
Fig 9.—Top, The tuberculoma in patient 1 (Fig 3) diagrammed on the cortical map is located the striate cortex than Holmes appre¬
more anteriorly than predicted by the Holmes map. Note that the lesion must cross the V1/V2 ciated (compare Figs 1 and 8). The
frontier because the patient's scotoma bordered the vertical meridian. Center, Diagram of right areas devoted to the representation of
visual field defect in patient 3 is plotted on the map of the left visual cortex (shaded region
indicates infarcted cortex). Macular sparing reached 2° along the upper vertical meridian, 2.5°
the central 1° of vision and the entire
along the horizontal meridian, and 4° along the lower vertical meridian (see Fig 6, inset). The temporal crescent are roughly equal in
amount of intact cortex is considerably greater than the Holmes map indicates. Bottom, The the human striate cortex. This ex¬
integrity of most of the striate cortex (shaded area) is tested by examining only the central 30° of plains why visual field deficits of corti¬
vision, because the representation of central vision is so highly magnified. cal origin limited strictly to the tempo¬
ral crescent are so rare. Few lesions
are likely to fall precisely within the
diminutive confines of the temporal
crescent representation in the striate
cortex. Most lesions involving the tem¬
poral crescent representation will also
involve the optic radiations or periph¬
eral binocular cortex, thereby result¬
ing in bigger field defects.
Human Cortical Magnification Factor
The linear magnification factor
(Miij^J in the striate cortex is inversely
proportional to eccentricity (E).2S
There is no universal agreement on the
correct equation for linear magnifica¬
tion factor (millimeters of cortex/de¬
gree of visual field) in macaque striate
cortex. The following expression is a
reasonable approximation, based on
published formulas1213·16·23'26'27:
12
Monkey: Mu, linear
# + 0.75,
where E is eccentricity in degrees.
This equation applies to the macaque
striate cortex, which has a mean sur¬
face area of 1200 mm2. 12 The human
striate cortex averages 2500 mm2,
greater in area by a factor of 2.08.
If our revision of the Holmes map is
correct, the magnification formula for
the macaque striate cortex can be
adapted to the dimensions of the hu-
1. Inouye T. Die Sehstorungen bei Schussverlet-
zungen der kortikalen Sehsphare. Leipzig, Germa-
ny: W Engelmann; 1909.
2. Glickstein M. The discovery of the visual cor-
tex. Sci Am. 1988;259:118-127.
3. Holmes G, Lister WT. Disturbances of vision
from cerebral lesions with special reference to the
cortical representation of the macula. Brain.
1916;39:34-73.
4. Holmes G. Disturbances of vision by cerebral
lesions. Br J Ophthalmol. 1917;2:353-384.
5. Holmes G. The organization of the visual cor-
tex in man. Proc R Soc Lond Series B (Biol).
1945;132:348-361.
6. Orr LS, Schatz NJ, Gonzalez CF, Savino PJ,
Corbett JJ. Computerized axial tomography in
evaluation of occipital lobe lesions. In: Smith JL,
ed. Neuro-ophthalmology Update. New York, NY:
Masson Publishing USA Inc; 1977:351-367.
7. McCauley DL, Russell RWR. Correlation of
CAT scan and visual field defects in vascular lesions
of the posterior visual pathways. J Neurol Neuro-
surg Psychiatry. 1979;42:298-311.
8. Kattah JC, Dennis P, Kolsky MP, Schellinger
D, Cohan SL. Computed tomography in patients
with homonymous visual field defects: a clinico-
radiologic correlation. Comput Tomogr. 1981;
5:301-312.
9. Spector RH, Glaser JS, David NJ, Vining DQ.
Occipital lobe infarctions: perimetry and computed
tomography. Neurology. 1981;31:1098-1106.
10. Talbot SA, Marshall WH. Physiological
studies on neural mechanisms of visual localization
and discrimination. Am J Ophthalmol. 1941;
24:1255-1263.
11. Daniel PM, Whitteridge D. The representa-
tion of the visual field on the cerebral cortex in
man striate cortex. A correction factor
of 1.44 (2.081'2) must be incorporated in
the expression for linear cortical mag¬
nification factor in the human striate
cortex:
17 3
Human: Mine„= -
E+ 0.75.
This formula gives a value for linear
cortical magnification of 9.9 mm/de¬
gree at 1° eccentricity, 3.0 mm/degree
at 5°, and 1.6 mm/degree at 10°. These
figures are in good agreement with
estimates of the human cortical magni¬
fication factor obtained by positron
emission tomography2" and by mapping
phosphenes evoked by direct electrical
stimulation.29'30
If we assume that human linear cor¬
tical magnification is isotropie (see
Tootell et al16 for a detailed discussion
of this issue), the above formula can be
squared to yield an expression for are-
al cortical magnification factor (milli¬
meters squared/degree squared):
Human: M„eal 300/(£ + 0.75)2.
=
Integration of this formula over the
visual field coordinates of any scotoma
will provide the size in millimeters
squared of the corresponding cortical
lesion. In practice, it is easier to obtain
this information by referring directly
References
monkeys. J Physiol (Lond). 1961;159:203-221.
12. Van Essen DC, Newsome WT, Maunsell
HR. The visual field representation in striate cor-
tex ofthe macaque monkey: asymmetries, anisotro-
pies, and individual variability. Vision Res.
1984;24:429-448.
13. Dow BM, Vautin RG, Bauer R. The mapping
of visual space onto foveal striate cortex in the
macaque monkey. J Neurosci. 1985;5:890-902.
14. Spalding JMK. Wounds of the visual path-
way, II: the striate cortex. J Neurol Neurosurg
Psychiatry. 1952;15:169-183.
15. Stensaas SS, Eddington DK, Dobelle WH.
The topography and variability of the primary visu-
al cortex in man. J Neurosurg. 1974;40:747-755.
16. Tootell RBH, Switkes E, Silverman MS,
Hamilton SL. Functional anatomy of macaque stri-
ate cortex, II: retinotopic organization. J Neurosci.
1988;8:1531-1568.
17. Stone J, Leicester J, Sherman SM. The naso-
temporal division of the monkey's retina. J Comp
Neurol. 1973;150:333-348.
18. Bunt AE, Minckler DS, Johanson GW. Dem-
onstration of bilateral projection of central retina of
the monkey with horseradish peroxide neuronog-
raphy. J Comp Neurol. 1977;226:544-564.
19. Leventhal AG, Ault SJ, Vitek DJ. The naso-
temporal division in primate retina: the neural
bases of macular sparing and splitting. Science.
1988;240:66-67.
20. Fukuda Y, Sawai H, Watanabe M, Wa-
kakuwa K, Morigiwa K. Nasotemporal overlap of
crossed and uncrossed retinal ganglion cell projec-
tions in the Japanese monkey (Macaca fuscata). J
Neurosci. 1989;9:2353-2373.
21. Smith CG, Richardson WFG. The course and
distribution of the arteries supplying the visual
to the map shown in Fig 8, bottom left.
When Inouye and Holmes published
their original maps, little was known
about the cortical representation of the
visual field in nonhuman primate spe¬
cies. When judged in this context,
their maps were remarkably accurate.
It would be surprising if their maps,
based on clinical data collected during
the early part of this century, did not
eventually require some modification.
With the advent of magnetic resonance
imaging, a technique with sufficient
resolution is finally available to permit
direct validation of the Inouye and
Holmes maps. Our analysis indicates
that their maps underestimated the
magnification of central vision in the
striate cortex. We suggest a revised
map based on visual field-magnetic
resonance correlation that brings the
human map into agreement with pub¬
lished data obtained from laboratory
investigations in closely related Old
World primate species.
This investigation was supported by the Heed
Ophthalmic Foundation and the Richard G. Sco-
bee Memorial Fellowship (J.C.H.), Chicago, 111.
Joan Weddell provided exceptional help prepar¬
ing the illustrations. Michael P. Stryker, PhD,
and Roger B. H. Tootell, PhD, gave comments on
the manuscript.
(striate) cortex. Am J Ophthalmol. 1966;61:1391\x=req-\
1396.
22. Yiannikas C, Walsh JC. The variation of the
pattern shift visual evoked response with the size of
the stimulus field. Electroencephalogr Clin Neuro-
physiol. 1983;55:427-435.
23. LeVay S, Connolly M, Houde J, Van Essen
DC. The complete pattern of ocular dominance
stripes in the striate cortex and visual field of the
macaque monkey. J Neurosci. 1985;5:486-501.
24. Horton JC, Dagi LR, McCrane EP, de Mon-
asterio FM. Arrangement of ocular dominance col-
umns in human visual cortex. Arch Ophthalmol.
1990;108:1025-1031.
25. Schwartz EL. Computational anatomy and
functional architecture of striate cortex: a spatial
mapping approach to perceptual coding. Vision
Res. 1980;20:645-669.
26. Hubel DH, Freeman DC. Projection into the
visual field of ocular dominance columns in macaque
monkey. Brain Res. 1977;122:336-343.
27. Schein SJ, de Monasterio FM. Mapping of
retinal and geniculate neurons onto striate cortex of
macaque. J Neurosci. 1987;7:996-1009.
28. Fox PT, Miezin FM, Allman JM, Van Essen
DC, Raichle ME. Retinotopic organization of hu-
man visual cortex mapped with positron-emission
tomography. J Neurosci. 1987;7:913-922.
29. Cowey A, Rolls ET. Human cortical magnifi-
cation factor and its relation to visual acuity. Exp
Brain Res. 1974;21:447-454.
30. Dobelle WH, Turkel J, Henderson DC, Ev-
ans JR. Mapping the representation of the visual
field by electrical stimulation of human cortex. Am
J Ophthalmol. 1979;88:727-735.