HOMONYMOUS CENTRAL QUADRANTANOPIA
CAUSED BY AN EXTRASTRIATE (V2/V3)
INFARCTION: A CASE REPORT
Shu-Fang Lin,1* Yu-Ting Kuo,2* Fang-Ling Chang,1 and Rong-Kung Tsai1,3
Department of Ophthalmology, Buddhist Tzu-Chi General Hospital, and Departments of
2
Medicine, and 3Ophthalmology and Visual Science, Tzu-Chi University, Hualien, Taiwan.
1

A 66-year-old Taiwanese aboriginal male had complained of right-side blurred vision for 2
months, especially when reading. He had a 10-year history of hypertension and cardiovascular
disease. His best-corrected visual acuity was 20/25 in each eye. Ophthalmoscopy revealed asymmetrical cupping, but a normal disc. Humphrey perimetry showed an upper homonymous paracentral quadrantanopic defect. Brain magnetic resonance imaging showed an infarction in the
left lower calcarine area over the extrastriate (V2/V3) cortical area and a narrowing of the left
middle and posterior cerebral arteries due to severe arteriosclerosis.

Key Words: calcarine fissure, extrastriate cortex, magnetic resonance
image, quadrantanopia
(Kaohsiung J Med Sci 2008;24:430–5)

The striate cortex extends along the calcarine fissure
on the medial surface of the occipital lobe. The striate
cortex also extends anteriorly from the junction between the calcarine fissure and the parieto-occipital
sulcus to the occipital pole [1]. The first case of quadrantanopia was reported by Hun in 1887 [2]. One
century ago, Inouye reported the first retinotopic
map of the striate cortex based on his observations of
soldiers with brain injuries during the 1904–1905
Russo-Japanese War. Inouye proposed that the vertical meridian was represented along the margin of the
calcarine lips and the horizontal meridian was at the
base of the calcarine fissure [3]. Holmes reported a similar map a decade later, and presented clearly the topographic characteristics of the contralateral hemifield

Received: Nov 30, 2007 Accepted: Mar 11, 2008
Address correspondence and reprint requests to:
Dr Rong-Kung Tsai, Department of Ophthalmology, Buddhist Tzu-Chi General Hospital,
707, Section 3, Chung-Yang Road, Hualien 970,
Taiwan.
E-mail: rktsai@tzuchi.com.tw
*The first and second authors contributed equally to
this work.

430

of vision in the striate cortex [4]. According to Holmes’
proposed retinotopic organization, a V1-based visual
deficit restricted to one quadrant of the visual field
(that is, a homonymous quadrantanopia) with a clean
border along the horizontal meridian would be the result of a lesion that included either the upper or lower
lip of the calcarine sulcus extending precisely to, but
not beyond, the horizontal meridian [4]. The upper
lip of the calcarine fissure represents the lower visual
fields and the lower lip represents the upper visual
fields [1]. Logically, Holmes’ statement was right and
is well accepted, but practically, it is not easy to imagine how such a lesion can sharply respect the winding
nature of the calcarine fissure and result in homonymous quadrantanopia.
Based on magnetic resonance imaging (MRI) evidence, Horton and Hoyt proposed another theory of
cortically-based homonymous quadrantanopia, whereby the lesion occurs in the extrastriate cortex, rather
than in the striate cortex. They reported that an early
extrastriate visual area within a hemisphere, such as
V2, V3 or V4v, represents a single quadrant of the visual
field [5,6]. In animal studies on monkeys, the extrastriate visual striate cortex (V2) completely surrounds
Kaohsiung J Med Sci August 2008 • Vol 24 • No 8
© 2008 Elsevier. All rights reserved.

the primary striate cortex (V1), except for the anterior
part, where the temporal crescent is located. The representation of the vertical meridian is located between
V1 and V2. Extrastriate visual area 3 (V3) is an area
around V1 and V2 that forms a horizontal meridian
with V2 and the vertical meridian delimiting the outer
border of V3. Thus, V2 becomes a mirror image of V1,
and shares the representation of the vertical meridian;
V3 is a mirror image of V2 and shares the representation of the horizontal meridian; furthermore, the outer
perimeter of V3 is defined by the vertical meridian [7].
Horton and Hoyt proposed that, in humans, the
horizontal and vertical meridians are represented in
not only the V1 area, but also in V2 and V3 [5,6]. This
proposal has been further supported by another report
that showed a positive correlation between anatomic
location based on functional MRI and the model proposed by Horton and Hoyt [8].
In this paper, we report a case with a unique
homonymous central quadrantanopic defect due to
an occipital lobe infarction for which, based on MRI
studies, the damage was mainly confined to a V2/V3
extrastriate lesion.

CASE PRESENTATION
The patient was a 66-year-old Taiwanese aboriginal
man with hypertension and hyperlipidemia who had
received an operation for a coronary artery bypass

30

graft due to severe triple vessel disease. The patient
had suffered from blurred vision in the right eye for
about 2 months. The blurring condition had persisted,
and was affecting his reading ability. On ocular examination, visual acuity was 20/25 in both eyes with best
correction. Slit lamp biomicroscopy revealed a mild
cataract and a silent anterior segment in each eye.
The intraocular pressures were 17 mmHg OD and
16 mmHg OS. The pupils were equal without any relative afferent papillary defect. Fundoscopy revealed
slightly enlarged cupping, but a normal neuro-rim.
On examination, the visual field was found to be
grossly intact by the confrontation test, but analysis
using Humphrey perimetry with a central 30–2 threshold program revealed a right upper homonymous
central quadrantanopia with macula splitting; this
respected the horizontal and vertical meridians and
was limited to the central 10 degrees in both eyes.
The basic data in the visual field report were: in both
eyes, fixation losses 0/17; false POS errors 0%; false
NEG errors 0%; mean deviation −5.38 dB (OD) and
−3.74 dB (OS) and PSD 4.11 dB (OD) and 4.62 dB (OS)
(Figure 1).
After the tentative diagnosis of a left occipital lobe
lesion, the patient was subjected to brain MRI, which
revealed an infarction of the occipital lobe with the
lesion being 21 mm in length, 19 mm in width and
12 mm thick. The lesion was located in the V2/V3
cortical area below the lower lip of the calcarine sulcus (V1) and adjacent to the posterior occipital pole.

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Figure 1. Humphrey perimetry (central 30–2 threshold program) revealed a right-upper homonymous scotomatous defect of 10° with
macula splitting that respected the horizontal and vertical meridians.
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Extrastriate quadrantanopia

Brain magnetic resonance angiography (MRA) also
showed a narrowing of the left middle and posterior
cerebral arteries due to severe arteriosclerosis (Figure
2). Although the patient did not have other obvious
neurologic signs, he was referred to the neurological
department for further medical care of the stroke.

DISCUSSION
The striate cortex can be further classified into anterior, intermediate and posterior parts. The anterior
part lies adjacent to the parieto-occipital fissure and
reflects the temporal crescent of the contralateral
visual field. The posterior lesions are located in the

posterior 50–60% of the striate cortex, which includes
the occipital pole and operculum and represent the
central macula area of vision [9].
Over time, the Holmes’ map has been modified to
reflect reality, with the foveal region occupying more
striate cortex of the occipital lobe than the peripheral
area. In macaque monkeys, the central 15° of vision
fills about 70% of the total surface area of the striate
cortex. In human studies, 25% of the surface area of
striate cortex presents the central 15° [3–5]. Another
study has reported that the central 10° of the visual
field is represented in humans by at least 50–60% of
the posterior striate cortex [10]. Our patient’s visual
field defect also showed a characteristic magnification
of the macula map in the striate cortex. The infarcted

A

B

C

D

Figure 2. (A) T2-weighted coronal magnetic resonance imaging (MRI) documents an area of infarction (arrow) below the lower lip of
the left calcarine sulcus (arrowhead) with V1 relatively spared. (B) T2-FLARE image of the left parasagittal sections shows an infarct
(arrow) below the lower bank of the calcarine sulcus, specifically an extrastriate lesion (V2/3). (C) T2-weighted axial MRI shows an
increased signal (arrow) in the left calcarine bank along the interhemispheric fissure. (D) Brain magnetic resonance angiography
shows a narrowing of the left middle and posterior cerebral arteries due to severe arteriosclerosis.

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S.F. Lin, Y.T. Kuo, F.L. Chang, and R.K. Tsai

lesion measured 21 mm in length (about half the
length of the calcarine fissure) in the MRI images, but
the quadrantanopia defect affected only 10° of the
central visual field.
Daniel and Whitteridge invented the term “linear
magnification factor” to refer to the millimeters of cortex representing 1° of visual field at any given eccentricity (E). They also reported a ratio of more than 40:1
between the fovea and periphery (60° eccentricity).
An advanced formula covering the visual field coordinates of a scotoma will provide the size in millimeters squared of the corresponding cortical lesion, which
for humans is Marea = 300/(E + 0.75)2 [11]. According to
the formula, a lesion with an area of 2.59 cm2 should
be found in the cortex of our patient. Based on the
MRI image obtained in this study, the area of the
defect was about 2.5 cm2.
The posterior pole of the occipital lobe is supposed
to have a dual blood supply with collateral circulation from the middle and posterior cerebral arteries;
this has been proposed to be a macula-sparing phenomenon and can be observed in cases with a small
infarct lesion and without mass compression. Maculasparing types of occipital lobe lesions will occur when
a lesion is located at the occipital pole and operculum,
because the occipital pole and operculum are supplied
by the posterior temporal or parieto-occipital branch
of the posterior cerebral artery, or an occipital branch
of the middle cerebral artery; the presence of such
collateral circulation will preserve the function of the
occipital pole. However, in 50% of normal brains, the
entire striate cortex, including the occipital pole, is
supplied by the calcarine branch of the posterior cerebral artery, and macula splitting occurs after a vascular infarct in such patients [9]. In our patient, MRA
demonstrated severe narrowing of the middle cerebral artery and the posterior cerebral artery, and these
factors may have added to the ischemic change induced in the occipital pole and delayed re-perfusion
from the collateral circulation. The presence of these
factors might explain the macula-splitting character
of the visual field defect in our patient.
The lower striate cortex is more vulnerable to ischemic damage. The characteristic vascular anatomy
and poor development of the collateral circulation in
the lower cortical area may explain this area’s vulnerability to infarcts. The mechanisms underlying such
infarcts include embolism from cardiac disease and
plaques in the vertebrobasilar system [5].
Kaohsiung J Med Sci August 2008 • Vol 24 • No 8

Wong and Sharpe compared the accuracy of manual kinetic (tangent screen and the Goldmann perimeter) and automated static perimetry (Humphrey
perimeter) among patients with occipital lobe lesions
[12]. After comparing the results with those from
MRI, all three perimetric techniques were found to be
satisfactory screening tests for the detection of occipital lesions. They also proposed that the tangent
screen and Goldmann perimetry approaches provided more information about the location and extent of
lesions in the postgeniculate visual pathway than the
Humphrey perimeter method [12]. However, clinically, the Humphrey perimeter approach is still the
most common, general, fast and reliable screening
tool used for the visual pathway. Furthermore, it is
not easy to detect a homonymous paracentral quadrantanopic defect as occurred in our patient using
the confrontation method only. Thus, autoperimetry
still has value when detecting a specific pattern of
defect.
In a large survey of homonymous hemianopias,
homonymous scotomatous defects, such as homonymous central quadrantanopia with macula splitting,
made up 12% of the total number of events. The main
lesion sites for a homonymous scotomatous defect
were the occipital lobe (50%), optic radiation (30%),
and the optic tract (10%) [13]. However, a superior
homonymous quadrantanopia caused by a temporal
lobe lesion with damage to Meyer’s loop would induce
an optic radiationally-filled defect. The characteristics
of such a visual field defect would be incongruous
with a sloping border and a failure to respect precisely the horizontal meridian. Homonymous quadrantanopia respecting the horizontal meridian ought
to indicate striate or extrastriate cortical disease [10].
The precise MRI images of the coronal and sagittal
sections obtained in this case provided better spatial
resolution than a computed tomography scan, and
this allowed better correlation with the visual field
defect [14,15].
An infarct of the extrastriate cortex over the V2/V3
area would result in a homonymous central quadrantanopia. Our MRI studies provide evidence of a V2/V3
lesion with relative sparing of V1. The present homonymous central quadrantanopic defect is relatively
small, but it has affected reading ability. Variation in
the vessels supplying the visional cortex across the
posterior occipital lobe may contribute to the maculasplitting phenomenon in our patient.
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Extrastriate quadrantanopia

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S.F. Lin, Y.T. Kuo, F.L. Chang, and R.K. Tsai

林淑芳

1

1

郭雨庭

2

張芳綾

佛教慈濟綜合醫院

慈濟大學

2

醫學系

3

1

蔡榮坤

1,3

眼科

眼暨視覺科學

一位六十六歲原住民男性主訴近兩個月以來右眼視力模糊，尤其是在閱讀時。病患有
高血壓及心臟病約十年之久，兩眼最佳矯正視力均為零點八，直接眼底鏡檢查發現兩
側視神經盤之視杯大小不對稱，視野檢查發現有雙眼同側中心上象限盲，其來源由腦
部核磁共振影像推測為左大腦枕葉距狀溝下方之第二及第三皮質處因動脈粥狀硬化所
引致之中及後大腦動脈狹窄所造成之梗塞。

關鍵詞：距狀溝，紋外皮質，核磁共振造影，象限偏盲
( 高雄醫誌 2008;24:430–5)

收文日期：96 年 11 月 30 日
接受刊載：97 年 3 月 11 日
通訊作者：蔡榮坤醫師
佛教花蓮慈濟綜合醫院眼科
花蓮市 970 中央路三段 707 號
Kaohsiung J Med Sci August 2008 • Vol 24 • No 8

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第二及第三皮質病灶引致的同側中心象限盲
─ 病例報告