CASE REPORT

Case Series: Bilateral Homonymous Visual Field Defects Due to
Bilateral Ischemic Strokes
Eleni Papageorgiou, MD, PhD,1,2* Nikolaos Anthis, MD,3 Theodora Stathi, MD,2 Evangelia Tsironi, MD, PhD,2
and Ioannis Asproudis, MD, PhD3

SIGNIFICANCE: Bilateral strokes are rare and should be considered when patients present with bilateral visual
field loss characterized by patterns consistent with right and left-sided homonymous visual field defects.
Perimetry, dilated funduscopy, and immediate neuroimaging are mandatory for diagnosis, because patients may
present with vague symptoms. These cases reflect the retinotopic features of the striate cortex.
PURPOSE: The purposes of this study were to describe the unusual presentation of bilateral homonymous visual field
defects in three patients with bilateral ischemic strokes and to discuss the clinical and neuroanatomical correlations.
CASE REPORTS: Neuro-ophthalmological examination including perimetry and brain magnetic resonance imaging (MRI) was performed in three patients with bilateral homonymous scotomas. Two of three patients presented
with superior altitudinal hemianopia, resulting from right and left homonymous superior quadrantanopia due to
bilateral occipital strokes below the calcarine fissure. A 57-year-old man (patient 1) with a history of atrial fibrillation presented with driving difficulties. Perimetry revealed bilateral superior altitudinal hemianopia. Brain MRI
demonstrated a subacute right occipital stroke and a chronic left occipital stroke, both inferior to the calcarine fissure.
An 83-year-old woman (patient 2) presented with reading disorders. Perimetry showed a left incomplete homonymous
hemianopia and a right horizontal wedge-shaped homonymous scotoma. Brain MRI showed a chronic ischemic stroke
in the left occipital lobe and acute ischemia in the right thalamus. A 40-year-old man (patient 3) was referred with
headache, disorientation, and bilateral blurry vision. Perimetry showed bilateral superior altitudinal hemianopia,
and MRI demonstrated acute bilateral occipital ischemia. Patients 1 and 2 suffered sequential bilateral strokes
and were not aware of the initial scotoma, whereas patient 3 presented with bilateral concurrent strokes.
CONCLUSIONS: Bilateral homonymous visual field defects due to bilateral strokes are rare. Patient history, a careful neuro-ophthalmological examination, and correlation of visual field defect patterns with neuroimaging should
prompt the clinician to the presence of this unique entity.
Optom Vis Sci 2018;95:1077–1082. doi:10.1097/OPX.0000000000001294
Copyright © 2018 American Academy of Optometry

Field defects respecting the vertical midline indicate chiasmal
or retrochiasmal brain damage, with the occipital lobe being the
most common lesion location and stroke being the most common
etiology.1 Unilateral damage to the retrochiasmal visual pathway
results in homonymous visual field defects, which affect corresponding areas of the contralateral visual field in both eyes and
are found in approximately 8% of stroke patients and 25% of
traumatic brain injury patients.2 Bilateral damage to the retrochiasmal
visual pathway causes bilateral homonymous scotomas, which affect
both visual hemifields in both eyes.1 Depending on the degree
and the affected site of the optic pathway, various clinical types
of bilateral homonymous visual field defects have been described,
which are rare and have been infrequently reported.3–12 A previous
study has reported that only 6% in a large group of patients with
homonymous hemianopias had bilateral visual field loss, and
up-to-date most published studies represent single case reports.1
There have been eight case reports of bilateral superior altitudinal
hemianopia caused by occipital lobe lesions3; however, the extent of the lesions inside the visual cortex was not always evaluated in those previously reported patients.3 Similarly, in an older
report of 15 patients with bilateral homonymous hemianopia,
neuroimaging was performed in only five patients.4 There are also
some additional sporadic case reports of altitudinal hemianopia,
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Author Affiliations:
1
Ophthalmology Group,
University of Leicester, Leicester,
United Kingdom
2
Ophthalmology Department,
University of Thessaly,
Larisa, Greece
3
Ophthalmology Department,
University Hospital of Ioannina,
Greece
*e_papage@yahoo.com

resulting from a combination of bilateral superior or inferior
homonymous quadrantanopia.5–7
We here report detailed clinical and radiological findings of
three additional cases of bilateral homonymous visual field defects,
two patients presenting with superior altitudinal hemianopia,
resulting from a combination of right and left superior homonymous quadrantanopia, and a third one with bilateral incomplete
homonymous hemianopia. Based on magnetic resonance imaging
findings, we evaluated the extent of the lesions affecting the visual
pathway and discussed the correlation between the location of the
lesions and visual field defects in our patients. The clinical and neuroanatomical correlations in those rare cases aim to further enhance
our understanding of the retinotopic features of the striate cortex.

METHODS
Three patients presented with acute visual problems, all of
which ultimately represented the same underlying cause. All patients underwent neuro-ophthalmological examination, including best-corrected visual acuity, intraocular pressure, slit-lamp
biomicroscopy, and both direct and indirect funduscopy. Visual
fields were assessed with standard automated static perimetry,

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Bilateral Hemianopia — Papageorgiou et al.

FIGURE 1. Humphrey 24-2 static automated perimetry of patient 1. There is bilateral superior homonymous quadrantanopia, which resembles superior
altitudinal visual field defects.

using the central 24-2 and central 30-2 threshold test of the Humphrey field analyzer (Humphrey Field Analyzer, 24-2 and 30-2 Test
Protocol; Carl Zeiss Meditec, Dublin, CA). In addition, magnetic
resonance imaging with gadolinium was performed. All patients
underwent neuropsychological testing for visual hemineglect,
visual object agnosia, simultanagnosia, and prosopagnosia.
No evidence of visual agnosias was found. The study was performed according to the Declaration of Helsinki. No identifiable
health information was included in this case series.

RESULTS
Patient 1
A 57-year-old man presented with driving difficulties for the
past 2 days. His medical history was remarkable for atrial fibrillation;
he had suffered an ischemic stroke 6 months prior and had been on
antihypertensives and aspirin since then. He was not aware of any
previous ophthalmological abnormalities and had not seen an eye
care practitioner for the past 2 years. On examination, the patient's
best-corrected visual acuity was 20/20 in both eyes, with normal
ocular motility and normal color vision. Confrontation visual field
testing revealed bilateral superior visual field defects, which was
confirmed with Humphrey 24-2 automated perimetry as bilateral
superior altitudinal hemianopia that respected the horizontal
midline (Fig. 1). Slit-lamp biomicroscopy and dilated funduscopy
did not reveal any pathological findings. In particular, the optic discs
appeared pink with sharp margins and a cup-to-disc ratio of approximately 0.3. No optic disc pallor, edema, hemorrhage, neuroretinal
rim damage, or changes of the peripapillary region, which could imply
glaucomatous or ischemic optic nerve damage, were noted.
Fluid-attenuated inversion recovery magnetic resonance imaging demonstrated bilateral occipital ischemic strokes inferior to
the calcarine fissure, corresponding to bilateral superior homonymous quadrantanopia that respected the horizontal midline and
led to bilateral altitudinal field loss (Fig. 2). There was a subacute
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FIGURE 2. Axial fluid-attenuated inversion recovery magnetic resonance
imaging of patient 1. There are bilateral lesions of the inferior occipital
lobe. There is a subacute right posterior cerebral artery territory infarct involving the right posterior temporal lobe and occipital cortex (white arrow)
and an old left posterior cerebral artery territory infarct (black arrow).

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Bilateral Hemianopia — Papageorgiou et al.

right posterior cerebral artery territory infarct involving the right
medial/posterior temporal lobe, occipital cortex, and pulvinar of
the right thalamus, with a small amount of parenchymal hemorrhagic transformation (Fig. 2, white arrow). The infarct showed
mild enhancement after gadolinium injection, which was also
suggestive of a subacute stroke. In addition, there was a mature previous left posterior cerebral artery territory infarct with
ex vacuo expansion of the occipital horn of the left lateral ventricle
(Fig. 2, black arrow). The patient was admitted to the hospital for
cardiac and neurologic monitoring and was started on dipyridamole
and atorvastatin.

Patient 2
An 83-year-old woman presented with a 24-hour history of
reading disorders and problems in finding the beginning of lines.
She had a history of a cerebral stroke 1 year ago, and her medical
history was remarkable for diabetes mellitus, hypertension, and hyperlipidemia. Slit-lamp examination and dilated funduscopy were
normal. Humphrey automated static 24-2 perimetry showed a left
incomplete incongruous homonymous hemianopia and a right horizontal homonymous sectoranopia with macular sparing (Fig. 3).
T2-weighted and fluid-attenuated inversion recovery magnetic resonance imaging showed an acute ischemic infarction of the right
thalamus (Fig. 4A, white arrow) and an old infarct of the left occipital lobe (T2 and fluid-attenuated inversion recovery magnetic resonance imaging, Fig. 4A, black arrow, and Fig. 4B). Post-contrast
magnetic resonance imaging showed a mild peripheral enhancement in the right thalamus consistent with the acute infarction.
The patient was started on oral metformin, chlorthalidone, benazepril,
clopidogrel, and atorvastatin under regular cardiological evaluations.

Patient 3
A 40-year-old man was referred with a 24-hour history of headache, disorientation, loss of short-term memory, and bilateral blurry
vision. His previous medical history was unremarkable. Slit-lamp
biomicroscopy and dilated funduscopy were unremarkable, but
Humphrey automated static 30-2 perimetry showed bilateral

superior altitudinal hemianopia, as a result of right and left superior
homonymous quadrantanopia (Fig. 5). T2-weighted magnetic
resonance imaging demonstrated acute bilateral ischemic infarctions in the posterior cerebral artery territory below the
calcarine fissure (Figs. 6A, B), leading to bilateral superior homonymous quadrantanopia. Post-contrast magnetic resonance imaging
showed gyral enhancement of the lesions bilaterally, suggestive of
acute ischemia. Because of his young age, the patient was referred
for cardiological evaluation. Carotid and vertebral artery Doppler
ultrasonography scans were normal, as was transesophageal
echocardiography, but Holter monitoring revealed premature ventricular and supraventricular contractions, and the patient was
started on oral clopidogrel (75 mg) daily. Thrombophilia screening
and autoantibody testing including anticardiolipin antibodies were
within normal limits.

DISCUSSION
Typically, unilateral lesions of the post-chiasmatic visual
pathway result in contralateral homonymous hemianopia or
quadrantanopia. Bilateral post-chiasmatic lesions result in
homonymous defects of both visual hemifields, as seen in the
presented patients.
Bilateral homonymous scotomas are relatively rare and constitute approximately 6% of homonymous visual field defects.1
Cerebrovascular accidents to the occipital lobe, such as infarction
and, less commonly, hemorrhage, are the most common cause,
followed by trauma and tumor.1,2 All three patients in the present
report had cardiovascular risk factors: atrial fibrillation (patient 1),
diabetes mellitus, hypertension, hyperlipidemia (patient 2), and
cardiac arrhythmia (patient 3). Usually, bilateral infarctions occur
sequentially, but in some cases, they can also occur simultaneously.1,2 Patients 1 and 2 had suffered consecutive bilateral
infarctions, whereas patient 3 presented with simultaneous
bilateral infarctions.

FIGURE 3. Humphrey 24-2 static automated perimetry of patient 2. Bilateral homonymous visual field defects, including a left incomplete homonymous
hemianopia and a right horizontal wedge-shaped incongruous homonymous scotoma with macular sparing.

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Bilateral Hemianopia — Papageorgiou et al.

FIGURE 4. Brain magnetic resonance imaging of patient 2. (A) Axial T2 magnetic resonance imaging demonstrates an old left posterior cerebral artery
infarct (black arrow) and an acute right paramedian thalamic infarction (white arrow). Blurring of the image is owing to motion artifacts. (B) Sagittal flair
magnetic resonance imaging shows the old left posterior cerebral artery infarct (black arrow).

Patients 1 and 3 had bilateral lesions of the occipital lobe below
the calcarine fissure, which led to bilateral superior altitudinal field
loss from a combination of right and left homonymous superior
quadrantanopia. According to the retinotopic organization described

by Horton and Hoyt,13 the primary visual cortex contains a topographic representation of the contralateral hemifield of vision.
The upper and lower visual quadrants are represented in the lower
and upper calcarine banks, respectively, separated by the horizontal

FIGURE 5. Humphrey automated static 30-2 perimetry of patient 3. There is bilateral superior altitudinal hemianopia resulting from bilateral superior
homonymous quadrantanopia.

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Bilateral Hemianopia — Papageorgiou et al.

FIGURE 6. Brain magnetic resonance imaging of patient 3. (A) Axial T2 magnetic resonance imaging demonstrates acute bilateral ischemic infarctions in the
posterior cerebral artery territory. (B) The infarctions are located below the calcarine fissure, as shown in sagittal T2 magnetic resonance imaging (black arrow).

meridian along the base of the calcarine fissure.13 The superior
altitudinal hemianopia of patients 1 and 3 is, namely, a combination of a right homonymous superior quadrantanopia and a left
homonymous superior quadrantanopia, resulting from occipital ischemic infarctions of the posterior cerebral artery inferior to the
calcarine fissure.12 Alternatively, if both lesions were located
above the calcarine fissure, the result would be an inferior
altitudinal hemianopia.
It is hypothesized that the lower striatal cortex is more sensitive
to ischemia because the upper cortex has a more developed collateral circulation.1 Rarely, bilateral superior altitudinal hemianopia
has been reported in multiple sclerosis.1 On the other hand, bilateral inferior altitudinal defects usually result from tumors and
traumas, such as bullet wounds. Bilateral inferior altitudinal visual
field defects have been also described after cardiac surgery
and Creutzfeldt-Jakob disease.9,11 Finally, crossed homonymous
quadrantanopias (“checkerboard” visual fields) present in lesions
of the superior occipital lobe (above the calcarine fissure) on one
side and the inferior occipital lobe (below the calcarine fissure)
on the opposite side.1 In summary, the acute onset, the good visual
acuity, and the normal fundus findings in patients 1 and 3 suggest
that the superior bilateral altitudinal hemianopia resulted from a
combination of right and left superior homonymous quadrantanopia,
which was caused by bilateral occipital infarctions. In addition, the
high congruence of the visual field defects is consistent with a lesion of the occipital lobe or the posterior visual radiation and makes
a pre-chiasmal or chiasmal cause unlikely.
Common pre-chiasmal causes of bilateral altitudinal hemianopias
include bilateral anterior ischemic optic neuropathy and bilateral
glaucomatous optic neuropathy, which are associated with abnormal
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optic disc findings. The onset of arteritic or nonarteritic anterior ischemic optic neuropathy is usually unilateral, and the condition is
accompanied by painless visual loss, optic disc edema, a relative
afferent pupillary defect, and an altitudinal visual field defect
(typically inferior).12 In addition, in bilateral anterior ischemic optic neuropathy, the altitudinal inferior defects are usually asymmetrical. Bilateral symmetrical altitudinal hemianopia in bilateral
anterior ischemic optic neuropathy or optic neuritis is extremely
rare.8 Bilateral altitudinal visual field defects have been also reported in bilateral glaucoma, optic nerve head drusen, and tilted
discs.14,15 Those conditions are not acute and can be diagnosed
on the basis of pathological optic disc findings.
Compressive chiasmal lesions, that is, sellar and suprasellar tumors, arteriosclerotic internal carotid arteries, and aneurysms of
the anterior cerebral artery, are rare but can also lead to bilateral,
inferior or superior, altitudinal hemianopias.12 Chiasmal lesions
are typically associated with asymmetrical visual acuity loss, optic
atrophy, and a relative afferent pupillary defect.8 Bilateral occipital
lesions can also lead to reduced visual acuity, which is, however,
symmetrical. In addition, in those cases (post-geniculate lesions),
the funduscopic findings are normal, and there is usually no relative afferent pupillary defect.9
Optical coherence tomography imaging can be useful as a supplementary diagnostic tool for assessing changes in the ganglion
cell layer–inner plexiform layer complex and the retinal nerve fiber
layer due to intracranial lesions at different locations within the visual pathway.16,17 A recent study of patients with intracranial lesions affecting the optic chiasm or the optic tract and/or lateral
geniculate nucleus showed that clinical abnormalities in those patients are more likely to demonstrate abnormalities of ganglion cell

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Bilateral Hemianopia — Papageorgiou et al.

layer–inner plexiform layer complex than global peripapillary retinal nerve fiber layer thickness and that papillomacular bundle
thickness measurement appears to be a valuable tool to detect abnormalities of the anterior visual pathways.16 Similar findings have
been described in patients with retrogeniculate lesions in the posterior visual pathway, who showed significant thinning of the ganglion cell layer in the projecting sector of the retina mapping to
the brain lesion.17
Patient 2 presented with a different pattern of bilateral homonymous
scotomas, comprising a left incomplete homonymous hemianopia and
a right horizontal wedge-shaped homonymous scotoma. The left
incomplete incongruous homonymous hemianopia was attributed
to an acute infarction of the right thalamus (Fig. 4A, white arrow).
Visual field defects in cases of thalamic infarcts have been described rarely and mainly comprise incongruous homonymous
hemianopias and complete homonymous hemianopias.1 In addition, the right horizontal sectoranopia in patient 2 corresponded
to an old left posterior cerebral artery infarction. Horizontal
sectoranopias, which lie along the horizontal midline, are rare
and are mainly encountered in lesions of the lateral geniculate
nucleus1; however, in patient 2, the underlying cause is damage
to the intermediate portion of the occipital lobe in the region of the
calcarine fissure, which has been described less frequently.2
Patient 2 also had macular sparing to the right hemifield, which
is associated with preservation of the occipital tip.13
Interestingly, patients 1 and 2 were not aware of the homonymous
visual field defects after the initial stroke, and they presented to the
ophthalmology department only after the second stroke, which
caused further deterioration of their visual field. Except for the

ARTICLE INFORMATION
Submitted: November 27, 2017
Accepted: June 23, 2018
Funding/Support: None of the authors have reported
funding/support.
Conflict of Interest Disclosure: None of the authors have
reported a financial conflict of interest.
Author Contributions and Acknowledgments: Conceptualization:
EP, ET, IA; Data Curation: EP, NA, TS; Formal Analysis: EP,
NA, TS, IA; Investigation: EP, NA, TS; Methodology: EP,
NA, IA; Project Administration: EP, ET, IA; Supervision:
ET, IA; Validation: EP, ET, IA; Visualization: EP;
Writing – Original Draft: EP, NA, TS; Writing – Review
& Editing: ET, IA.
Drs. Tsironi and Asproudis contributed equally to
this work.

REFERENCES
1. Zhang X, Kedar S, Lynn MJ, et al. Homonymous
Hemianopias: Clinical-anatomic Correlations in 904
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2. Gilhotra JS, Mitchell P, Healey PR, et al. Homonymous Visual Field Defects and Stroke in an Older Population. Stroke 2002;33:2417–20.

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visual symptoms, unilateral occipital lobe lesions are generally
not associated with other neurological problems. Hence, patients
are not always aware of the accompanying homonymous visual
field defects until they suffer a second event in the contralateral
hemisphere weeks to years later, causing a more pronounced visual
impairment. On the other hand, patient 3 presented in the acute
setting because he developed simultaneous bilateral infarctions
leading to bilateral superior altitudinal hemianopia.

CONCLUSIONS
Bilateral cerebral infarcts should be considered in acute, symmetrical, bilateral visual field defects, especially in cases with preserved visual acuity and unremarkable fundus findings. These
cases are rare and reflect the retinotopic features of the striate cortex. Patients may present with vague symptoms because homonymous visual field defects can be encountered as an isolated
finding and do not always clearly point toward the underlying cerebral lesion. A thorough clinical examination including perimetry
and dilated funduscopy will aid the clinician to promptly identify
unexplained vision loss due to bilateral homonymous scotomas.
Such dense visual field defects with no corresponding optic disc
or retinal abnormalities should indicate a need for prompt neuroimaging, as they may indicate bilateral homonymous hemianopias.
Efficient and rapid diagnosis of the exact type and cause of those
rare bilateral homonymous hemianopias remains crucial in modern
stroke therapy.

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14. Hu S, Smith ND, Saunders LJ, et al. Patterns of Binocular Visual Field Loss Derived from Large-scale Patient Data from Glaucoma Clinics. Ophthalmology
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9. Smith JL, Cross SA. Occipital Lobe Infarction after
Open Heart Surgery. J Clin Neuroophthalmol 1983;3:
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16. Zehnder S, Wildberger H, Hanson JVM, et al.
Retinal Ganglion Cell Topography in Patients with
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