Medical Hypothesis
-

Homonymous quadrantanopia respecting
the horizontal meridian
A feature of striate and extrastriate cortical disease
Robert M. McFadzean, FRCOpth; and Donald M. Hadley, PhD, FRCR

Article abstract--It has been proposed that honionymous quadrantanopic visual field loss that respects the horizontal
meridian is a pathognomonic sign of extrastriate cortical disease. However, two patients with this sign are reported- oiiv
with a rare striate and the other with an extrastriatal lesion of the visual cortex. It is therefore hypothesized that ;I
homonymous quadrantanopia respecting the horizontal meridian may indicate striate and/or extrastriate cortical disease
NEIJKOI,OC;Y 1997;49 1741-1746

In 1909 the first map of the representation of the
visual field in the occipital striate cortex was published’ in which the superior and inferior visual
fields were separated by the representation of the
horizontal meridian along the base of the calcarine
fissure. Initial reports of homonymous quadrantanopic visual field defects respecting the horizontal meridian concerned soldiers with penetrating injuries of
the cranium sustained in the First World War.2
These defects were the result of damage to the occipital striate cortex, and they shared the remarkable
distinguishing feature of a sharp and steep demarcation along the horizontal meridian. Six of the seven
original cases affected the superior bank of the calcarine fissure with a corresponding inferior homonymous yuadrantanopia, and in only one patient was a
superior homonymous quadrantanopia described.
The paucity of superior visual field loss was attributed to a likely fatal outcome in most inferior
calcarine traumatic lesions, owing to concomitant
laceration of the dural sinuses. These patients supported the concept that the superior and inferior visual fields were localized to the inferior and superior
calcarine banks respectively, separated by the representation of the horizontal meridian along the base
of the calcarine fissure. However, this proposal was
challenged when doubts were expressed about the
possibility of a traumatic lesion of one calcarine bank
leaving the other unharmed.
Such projectile
trauma would be required to respect the wavering
representation of the horizontal meridian in the base
of the calcarine fissure, a highly improbable scenario.
Subsequently, an additional report of two soldiers
trauinatized by a missile injury to the optic radia-

tion5 noted that the resultant homonymous quadrantanopia also respected the horizontal meridian,
giving rise to the postulate that fibers in the optic
radiation representing the superior and inferior visual fields were physically separated from each other
by a n anatomic interval. This interval would permit
respect for the horizontal meridian in the consequential visual field defect. Thus, a relatively irregular
lesion could nevertheless produce a well-defined quadrantanopia with a sharp horizontal border. Furthermore, other authors suggested that the anatomic
interval was due to splitting of the optic radiations
into superior and inferior divisions by the posterior
horn of the lateral ventricle:’ and the interposition of
macular fibers between those representing the superior and the inferior visual fields.4 Thereafter, homonymous quadrantanopias respecting the horizontal
meridian were attributed to lesions of the optic radiations, and superior or inferior striatal lesions were
thought to be characterized by a n irregular horizontal border. Unfortunately no anatomic evidence has
emerged to support this proposed anatomic interval.
Indeed, studies in the cat demonstrate that the optic
radiations form a continuous sheet of fibers without
separation of those fibers representing the superior
and inferior visual fields.6 Temporal lobe lesions
could damage Meyer’s loop, giving rise to a superior
homonymous quadrantanopia, and parietal lobe lesions produce a n inferior homonymous quadrantanopia, but such optic radiational field defects had
sloping borders that failed to respect precisely the
horizontal meridian and were often i n c o n g r ~ o u s . ~
Following a literature review of 57 patients with
homonymous quadrantanopia respecting the horizontal meridian and a n MR study of two patients, it

P’riini thv

L)cyiartmc!nts of Neuro-ophthalmology (Dr. McFadzean) and Neuroradiology (Dr. Hadley), Institute of Neurological Scicncrs, Glasgow, Scotland
Hiveivc4 Fi4wunry 7 , 1997. Accepted in final form July 7, 1Y97.
Atltlrcm correspondence and reprint requests to Dr. Robert McFadzean, Department of Neuro-ophthalmology, Institute of Neurological Sciences. Soul htwi
( k ~ n c r a lHospital. 1945 Govan Road, Glasgow, (Xi1 4TF.
Copyright 0 1997 by t h e American Academy of Nrurology

1741

Posterior view

Medial view

Figure 1. Schematic diagram of the occipital cortex showing the arrangement of Vl,V2,and V3.Most of Vl is buried within the calcarine fissure. (Reproduced with
permission of the authors and Oxford University Press.
From Horton JC, Hoyt WF. Quadrantic visual field defects. A hallmark of lesions in the extra-striate WZlV3)
cortex. Brain 1991;114:1703-1718.)

was proposed that such visual field loss was a hallmark of an extrastriate cortical lesion.BThe concept
was based on animal studies9-I4that demonstrated
that the extrastriate visual area 2 (V2) completely
surrounds the primary striate cortex (Vl), except anteriorly where the monocular temporal crescent is
represented (figure 1). The representation of the vertical meridian is shared along the common border
between V1 and V2 (figure 2). The extrastriate visual area 3 073) is similarly wrapped around V1 and
V2, with the representation of the horizontal meridian sharing a common border with V2 and the vertical meridian delimiting the outer border of V3 (see
figure 2). In this fashion, V2 and V3 are split along
the horizontal meridian into superior and inferior
calcarine banks, representing the inferior and superior quadrants respectively of the contralateral

Figure 2. Schematic m a p corresponding to figure 1 that
shows Vl,V2,and V3 within the occipital cortex. The horizontal mrridian ( H M ) is shown at the base of the calcarine fissure and defines the outer limit o f V2. The vertical
meridian N M ) defines the outer limits of V1 and V3.
(Adapted with permission of the authors and Oxford University Press. From Horton JC, Hoyt WF. Quadrantic visual field defects. A hallmark of lesions in the extra-striate
(V2tV3)cortex. Brain 1991;114:1703-1718.)
1742 NEUROLOGY 49

December 1997

hemifield of vision. In the macaque monkey, the representation of the horizontal meridian continues
from V1 into V2, but quickly splits a short distance
from central fixation to outline the periphery of V2,12
while V3 as it approaches the representation of the
fovea is probably discontinuous. l z l m Thus V2 becomes a mirror image of V1, sharing the representation of the vertical meridian; V3 becomes a mirror
image of V2, sharing the representation of the horizontal meridian; and the outer perimeter of V3 is
defined by the vertical meridian. Isoeccentricity contours appear to pass from V1 to V2 without interrupt i ~ n . ' ~Consequently
,'~
the visual field is continuously
represented along any isoeccentricity contour line
from V1 into V2 and V3. A lesion crossing the border
between V1 and V2 or V2 and V3 damages cortical
tissue sharing common retinotopic coordinates.
Therefore, a lesion traversing the border between V2
and V3 would be characterized by a contralateral
homonymous quadrantanopia with respect for the
horizontal meridian.8 Although such a lesion could
have irregular margins, the resulting visual field
loss would have a sharply defined, steep horizontal
border, provided it crossed the representation of the
horizontal meridian in the extrastriate cortex. This
hypothesis proposes that such a perimetric feature is
a hallmark of extrastriate disease.8
The present report concerns two patients, both of
whom demonstrated a n inferior homonymous
quadrantanopia respecting the horizontal meridian
a s a feature of striate disease in one patient and
extrastriate disease in the other.
Methods. Two patients with lesions affecting the occipital cortex were assessed using conventional Goldmann dynamic perimetry and MRI. Images of the occipital cortex
were obtained in the sagittal oblique axial plane (i.e., in
the plane of the calcarine fissure) and the oblique coronal
plane (i.e., at a right angle to the plane of the calcarine
fissure). Thus the anatomic relationship of the lesion to the
calcarine fissure was identified. After correlation of the
perimetric and imaging findings, a comparison was made
with previously reported clinical cases of homonymous
yuadrantanopic visual field loss respecting the horizontal
meridian and the available experimental evidence of the
representation of the visual field in the striatetextrastriate
occipital cortex. Particular attention was paid t o known
variation in the blood supply of the calcarine cortex.
Results. Patient 1. A 40-year-old man developed a
right occipital infarct affecting the superior bank of the
calcarine cortex and extending into the base of the calcarine fissure (figure 3). Goldmann dynamic perimetry demonstrated a left inferior homonymous quadrantanopia that
respected absolutely the horizontal meridian and did not
extend fully to the vertical meridian (figure 4).
Patient 2. A 48-year-old man developed a spontaneous
right occipital hematoma, which resolved, leaving cerebromalacia in the right superior extrastriate cortex (figure 5).
Goldmann dynamic perimetry demonstrated a left inferior
homonymous quadrantanopia with respect for the horizontal meridian (figure 6).

Figure 3. (A, B) (A) T1-weighted
(spin echo, 580114) 5-mm-thick oblique axial section parallel to the
calcarine fissure and (B) a highdefinition, T1-weighted, thin (1-mm)
3D-MPRAGE (1014; 12 deg) coronal
section at a right angle to the calcarine fissure shows a right striatal infarct (large arrowhead) localized to
the superior bank of the calcarine
cortex and extending to the base of
the calcarine fissure. The parietooccipital fissure is indicated by the
small arrowhead in the oblique axial
section (A).

Discussion. Patient 1appears to demonstrate that
it is possible for a lesion affecting the superior bank
of the calcarine fissure to produce a contralateral
inferior homonymous quadrantanopia respecting the
horizontal meridian, in spite of the irregular and
wavering course adopted by the base of the calcarine
fissure. The pathology in this patient was presumed
to be an occipital infarct and it is in its vascular
etiology that the explanation for the visual field configuration lies. The course and distribution of the
arteries supplying the visual cortex were studied in
32 normal brains,l8 when it was found that the whole
visual area, defined as the extent of the occipital
cortex in which the stria of Gennari is seen using a
dissector's loupe, was supplied by the calcarine artery alone in some individuals. More usually, there

were supplementary branches from one or more
other arteries, namely the posterior temporal and
the parieto-occipital branches of the posterior cerebral artery and the occipital branch of the middle
cerebral artery. The distribution of the calcarine artery was somewhat variable, but in six brains it was
found to divide into superior and inferior divisions
running longitudinally in relation to the calcarine
fissure. In two specimens these vessels appeared to
share equally in the supply of the visual area; in
other words, the superior calcarine bank was supplied solely by the superior division of the calcarine
artery and the inferior calcarine bank was supplied
solely by the inferior division of the calcarine artery,
with complete respect for the representation of the
horizontal meridian at the base of the calcarine fis-

Figure 4. A = left, B = right. Goldmann dynamic perimetry shows a left inferior homonymous quadrantanopia that respects the horizontal meridian but does not extend fully to the vertical meridian. Note sparing of the left temporal crescent corresponding to the intact striate cortex adjacent to the right parieto-occipital fissure (small arrowhead) in figure
3A. The V,,, isopter refers to the threshold determined using a 2,000-apostilb test spot measuring 64 mm2, and the ISe
isopter refers to a 100-apostilb test spot measuring 0.25 mm2. The hemispheric bowl is positioned 33 cm from the eye with
a background luminance of31.5 apostilb.
December 1997 NEUROLOGY 49 1743

Figure 5. (A, B) Tl-weighted (spin echo, 550114) 5-mm-thick right parasagittal (A)and coronal (B) sections show cerebromalacia in the right superior extrastriate cortex. Note sparing of the superior bank of the calcarine fissure (arrowhead).

sure. Consequently it was predicted that infarction
of the superior calcarine bank with such a blood supply would result in a contralateral inferior homonymous quadrantanopia respecting the horizontal
meridian, as in this case. Because it is not possible to
image clinically the stria of Gennari, it cannot be
stated conclusively that the infarction spared the extrastriate cortex. However, anatomic studies have
shown that the medial exposed striate cortex extends
5 to 10 mm superior and inferior to the calcarine
fissure, wider posteriorly than anteriorly, and tapering toward the junction of the parieto-occipital and
calcarine f i s ~ u r e s . ' ~The
J ~ width of this marginal
part of the striate cortex varies from specimen to

specimen with the depth of the calcarine fissure, and
with the presence and height of any gyri that may
cross its floor.18 In this case, the infarct did not extend onto the exposed medial striate cortex on MRI.
Furthermore the inferior homonymous quadrantanopia did not extend to the vertical meridian, indicating that the lesion did not cross the V W 2 border
(see figure 2). It can therefore be safely assumed that
this infarct was confined to the striate cortex.
At first sight it may seem surprising that other
cases of striate cortical infarction with a homonymous quadrantanopia respecting the horizontal meridian have not been reported, as vascular lesions in
this territory are not uncommon. However, in the

Figure 6. A = left, B = right. Goldmann dynamic perimetry shows a left inferior homonymous quadrantanopia with respect for the horizontal meridian. The v,, isopter refers to the threshold determined using a 1,000-apostilb test spot measuring 64 mm2, and the 13eisopter refers to a 315-apostilb test spot measuring 0.25 mm2. The hemispheric bowl is
positioned 33 c m from the eye, with a background luminance of 31.5 apostilb.
1744

NEUROLOGY 49 December 1997

previously mentioned anatomic study,I8 only two of
32 specimens demonstrated a n independent blood
supply to the superior and inferior calcarine banks
by an individual branch of the calcarine artery. In
the remaining specimens there was a n overlapping
supply of the superior and inferior calcarine banks
by several branches of the calcarine artery, by
parieto-occipital and/or posterior temporal branches
of the posterior cerebral artery, and by a n occipital
branch of the middle cerebral artery. Infarcts of any
of these vessels-the more common scenario-would
result in a visual field defect that failed to respect
the horizontal meridian. Other less common pathologies encountered in the calcarine fissure, such as
traumatic lesions, neoplasia, and abscesses, are extremely unlikely to respect the representation of the
horizontal meridian in the base of the fissure. So far
as we are aware, this is the first reported patient
with a striate lesion confined to one calcarine bank
causing a contralateral homonymous quadrantanopia respecting the horizontal meridian, but in view
of the blood supply of the striate cortex, its unique
nature is not surprising.
On the other hand, our second patient clearly illustrates the contention that extrastriate disease superior or inferior to the calcarine fissure may also
produce an inferior or superior contralateral homonymous quadrantanopia that respects the horizontal
meridian. Although the topography of V2 in the human visual cortex has not been defined, comparison
with animal experiments inevitably leads one to the
conclusion that the extent of the extrastriate infarct
in our second patient would cross the V 2 N 3 boundary, where the horizontal meridian is also represented (see figure 2),L)1420L2
MRI in the saggital and
oblique coronal planes clearly demonstrates that the
lesion stops well short of the calcarine fissure and
the striate cortex. This patient therefore supports
the extrastriate hypothesis.H
In the correlation of perimetric function with imaging morphology, it is important to obtain MR images of the occipital cortex in the saggital, oblique
axial (i.e., in the plane of the calcarine fissure), and
the oblique coronal planes (i.e., a t a right angle to
the plane of the calcarine fissure), as in this study.
The precise relationship of calcarine bank lesions to
the base of the calcarine fissure can be readily identified by this means.
Regrettably the literature contains few reports of
homonymous quadrantanopia of cortical origin correlated with neuropathologic findings, although the
case of Dr. Mallory, the renowned Boston pathologist, provides support for the extrastriate hypothesis.ll Mallory suffered an inferior calcarine bank
infarct, mainly involving the extrastriate cortex but
encroaching slightly into the V1 area. Perimetry
demonstrated a left superior homonymous quadrantanopia precisely respecting the horizontal meridian. Although it involved the inferior striate
cortex, this infarct did not extend histopathologically
into the depth of the calcarine fissure. Thus, respect

for the horizontal meridian was a reflection of involvement of the V 2 N 3 border (see figure 2).
In humans there is considerable variation in the
location and extent of the striate cortex'" and it is
not possible to recognize the stria of Genarri on MRI.
Because precise determination of the location of the
V 1 N 2 boundary is impossible clinically, there is a
requirement for further neuropathologic studies to
correlate perimetric, imaging, and autopsy findings.
Future functional imaging studies may help to evaluate the representation of the visual field in the
occipital cortex and the effect of lesions.
Thus, visual field loss in the form of a homonymous
quadrantanopia respecting the horizontal meridian
may reflect either striate and/or extrastriate occipital
cortical disease. Detailed analysis of perimetric and imaging findings in our two patients provides clinical support for animal experimental evidence of the structural
organization of visual areas V1, V2, and V3 in the
striate and extrastriate occipital cortex.

Acknowledgments
We are grateful to our neurologic and neurosurgical collcagucs for
referring these patients, to Ms. Rosalind Stanners for the illustrntions, and to Mrs. Susan Campbell for careful preparation of this
manuscript.

References
1. Inouye T. Die Sehstorungen bei Schussverlet-yuiigeri
tler
kortikalen Sehspare: Nach Beobachtungen a n Verwundeten
der letzten japanischen Kriege. Leipzig: W. Engelmann, 1909.
2. Holnies G, Lister W T . Disturbances of vision from cerebral
lesions, with special reference to the cortical representation of
the macula. Brain 1916;39:34-73.
3. Monbrun A. Le centre cortical de la vision e t les radiations
optiques. Les hemianopsies de guerre et la projection retinienne cerebrale. Arch Ophthalmol 1919;36:641-670.
4. Ronne H. Ueber Quadranthemianopsie und die Lage der
Makulafasem in der okzipitalen Sehbahn. Klin Monatsbl Augenheilk 1919;63:358-374.
5 . Holmes G. Disturbances of vision by cerebral lesions. Br J
Ophthalmol 1918;2:353-384.
6. Nelson SB, Le Vay S. Topographic organization of the optic
radiation of the cat. J Comp Neurol 1985;240:322-330.
7. Van Buren JM, Baldwin M. The architecture of the optic radiation in the temporal lobe of man. Brain 1958;81:15-40.
8. Horton JC, Hoyt WF. Quadrantic visual field defects. A hallmark of lesions in the extra-striate (VLN3) cortex. Brain 1991;
114:1703-1718.
9. Cragg BG. The topography of the afferent projections in tht.
circumstriate visual cortex of the monkey studied by tlic
Nauta method. Vision Res 1969;9:733-747.
10. Zeki SM. Representation of central visual fields in prestriatcl
cortex of monkey. Brain Res 1969;14:271-291.
11. Allman JM, Kaas JH. A representation of the visual field in
the caudal third of the middle temporal gyrus of the owl
monkey (Aotus triuirgutus). Brain Res 1971;31:85-105.
12. Van Essen DC, Zeki SM. The topographic organization of
rhesus monkey prestriate cortex. J Physiol 197S;277:193226.
13. Gattass R, Gross CG, Sandell J H . Visual topography of V2 i n
the macaque. J Comp Neurol 1981;201:519-539.
14. Weller RE, Kaas JH. Retinotopic patterns of connections of
area 17 with visual areas V-11 and MT in macaque monkrys.
J Comp Neurol 1983;220:253-279.
15. Zeki SM. The third visual complex of rhesus monkey prestriate cortex. J Physiol 1978;277:245-272.
16. Gattass R, Sousa APB, Gross CG. Visuotopic organization and
December 1997 NEURO1,OGY 49 1745

extent of V3 and V4 of the macaque. J Neurosci 1988;8:18311845.
17. Allnian J M , Kaas JH. The organization of the second visual
area (V11) in the owl monkey: a second order transformation
of the visual hemifield. Brain Res 1974;76:247-265.
18. Smith CG, Richardson WFG. The course and distribution of
the arteries supplying the visual (striate) cortex. Am J Ophthalmol 1966;61:1391-1396,
19. Stensaas SS, Eddington DK, Dobelle WH. The topography and
variability of the primary visual cortex in man. J Neurosurg
1974;40:747-755.
20. Burkhalter A, Felleman DJ, Newsome WT, Van Essen DC.

1746 NEUROLOGY 49 December 1997

Anatomical and physiological asymmetries related to visual
areas V3 and VP in macaque extra-striate cortex. Vision Res
1986;26:63-80.
21. Newsome WT, Maunsell JHR, Van Essen DC. Ventral posterior visual area of the macaque: visual topography and areal
boundaries. J Comp Neurol 1986;252:139-153,
22. Van Essen DC, Newsome WT, Maunsell JHR, Bixby JL. The
projections from striate cortex (V1) to areas V2 and V3, in the
macaque monkey: asymmetries, areal boundaries, and patchy
connections. J Comp Neurol 1986;244:451-480.
23. Polyak S. The vertebrate visual system. Chicago: University
of Chicago Press, 1957:708, 737.

Homonymous quadrantanopia respecting the horizontal meridian: A feature of
striate and extrastriate cortical disease
Robert M. McFadzean and Donald M. Hadley
Neurology 1997;49;1741-1746
DOI 10.1212/WNL.49.6.1741
This information is current as of December 1, 1997
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