Optometry (2006) 77, 82-87

Three presentations of monocular vision loss
Melissa E. Trego, O.D.,a,b and Jean Marie Pagani, O.D.a,c
a

The Eye Institute, Pennsylvania College of Optometry, Philadelphia, Pennsylvania; bCardiff University, School of
Optometry and Vision Sciences, Cardiff, Wales, United Kingdom; and cNemours Health Clinic, Wilmington, Delaware.
KEYWORDS:
Retinal emboli;
Carotid artery disease;
Transient ischemic
attack

Abstract
BACKGROUND: Carotid artery disease is estimated to affect 30% of persons older than 50. Risk factors
include hypertension, cigarette smoking, hyperlipidemia and diabetes mellitus. Symptoms ascribed to
carotid artery lesions with stenosis of the artery or plaque formation include monocular vision loss and
transient ischemic attacks. Patients can present with transient monocular vision loss as their initial
symptom.
CASE REPORTS: Three patients from a geriatric clinic in Wilmington, Delaware presented with
different complaints of vision loss with similar overall outcomes. Patient A was an 87-year-old woman
who presented with dimming of vision on extreme left head turn. Dilated fundus examination found a
retinal arterial emboli in the left eye (O.S.). Carotid duplex examination found 50% to 79% left internal
carotid stenosis with no hemodynamic stenosis of the right internal carotid. Patient B was a 78-year-old
woman who presented with a right superior altitudinal defect and transient vision loss in the right eye.
Dilated fundus examination found retinal arterial emboli in the right eye (O.D.). Carotid duplex
examination found 50% to 79% carotid stenosis in both the left and right internal carotids. Patient C
was an 84-year-old man who complained of a superior altitudinal visual field defect O.D. Dilated
fundus examination found a retinal arterial emboli O.D. Carotid duplex results showed calcified
atherosclerotic plaques present at the level of the common carotid artery bifurcations bilaterally, with
50% to 70% narrowing of the right internal carotid artery with no significant narrowing of the left
internal carotid artery.
CONCLUSIONS: These 3 presentations show that in patients older than 50 who present with chief
complaints of monocular vision loss, a differential diagnosis of carotid artery disease must be
considered. Patients who exhibit retinal arterial emboli are at increased risk for stroke and vascular
death. Appropriate measures for confirming a diagnosis include duplex ultrasound imaging, magnetic
resonance angiography (MRA), and carotid angiography. Surgical techniques such as carotid angioplasty and carotid endarterectomy may be recommended.
Optometry 2006;77:82-87

Carotid artery disease is estimated to affect 30% of
individuals older than 50. A number of vascular risk factors
have been associated with carotid disease including hypertension, cigarette smoking, diabetes mellitus, and hyperlipidemia.1-7 The retinal vasculature of the eye can provide an

Corresponding author: Jean Marie Pagani, The Eye Institute, 1200 W.
Godfrey Avenue, Philadelphia, Pennsylvania 19141.
E-mail: jpagani@pco.edu

excellent “window” for the analysis of the cerebral microvasculature. Any type of emboli (calcific, cholesterol, fibrinoplatelet) lodged within the retinal arterial system may
represent the potential for the presence of emboli elsewhere
within the cerebral or cardiovascular circulation.2-4 Patients
with carotid artery disease may present with monocular,
ipsilateral vision loss; transient vision loss; asymptomatic
retinal emboli; or central retinal artery occlusion. The detection of emboli as an initial presentation of an underlying

1529-1839/06/$ -see front matter © 2006 American Optometric Association. All rights reserved.
doi:10.1016/j.optm.2005.12.003

Trego and Pagani

Clinical Care

83

systemic disease may afford the opportunity for early intervention.1-3,6-7 In the following case presentations, all 3
patients presented with monocular vision loss with concurrent detection of retinal emboli warranting further carotid
evaluation, ultimately leading to the diagnosis of carotid
artery disease.

Case presentation 1 (Patient A)
Patient A was an 87-year-old woman who presented with a
chief complaint of blurry vision on extreme left head turn 3
months before her examination. Ocular history was remarkable for bilateral pseudophakia. Her systemic history was
remarkable for hypertension and hyperthyroidism. Patient A
had no known drug allergies and was taking hydrochlorothiazide and propylthiouracil for her systemic conditions.
Best-corrected visual acuities at distance were 20/40 in the
right eye (O.D.) and in the left eye (O.S.). Pupils, confrontation visual fields, and ocular motilities were within normal
limits. Slit lamp examination found scleromalacia and epithelial basement membrane dystrophy of the cornea in both
eyes (OU). Intraocular pressures were 18 mmHg O.D. and
14 mmHg O.S. Dilated fundus examination found cellophane maculopathy OU and a plaque at the bifurcation of
the inferior retinal arteriolar tree O.S. No carotid bruit was
heard on the left or right side. The patient was referred for
an immediate carotid workup, which included a carotid
duplex examination. Results of carotid studies showed 50%
to 79% stenosis of the left internal carotid artery with no
stenosis of the right internal carotid. The patient declined
surgery and is being monitored for ocular sequelae of
carotid artery disease.

Case presentation 2 (Patient B)
Patient B was a 78-year-old woman who presented with a
chief complaint of a “black spot” over her right eye and
transient visual loss O.D. Ocular history was remarkable for
pseudophakia OU, nonproliferative diabetic retinopathy
OU, and maculopathy OU. Her systemic history was remarkable for hypercholesterolemia, acne rosacea, hypertension, type II diabetes mellitus (for 10 years), and kidney
problems. Patient B was taking nifedipine, metoprolol,
aprazolam, atorvastatin, furosemide, glipizide, doxazosin,
and lisinopril for systemic conditions. Best-corrected visual
acuities at distance were 20/30 O.D. and O.S. Pupils and
ocular motilities were within normal limits. Confrontation
visual fields showed a superior altitudinal defect O.D. and
were full O.S. Slit lamp examination was unremarkable, and
intraocular pressures were 11 mmHg OU. Dilated fundus
examination found moderate nonproliferative diabetic retinopathy OU and a retinal plaque in the inferior arteriolar
tree O.D. (see Figure 1). The patient was referred for an
immediate carotid workup, which included a carotid duplex

Figure 1 Fundus exhibiting a Hollenhorst plaque in the inferior arteriolar tree. (Photo compliments of Jodi Pukl, O.D.)

examination. Results of carotid studies showed 50% to 79%
stenosis of both the left and right internal carotids. The
patient is being followed up by a vascular specialist and is
being monitored closely for ocular sequelae of carotid artery
disease.

Case presentation 3 (Patient C)
Patient C was an 84-year-old man who presented with a
chief complaint of not being able to see in his superior
field of vision O.D. for 2 weeks before his examination.
Ocular history was remarkable for pseudophakia and
nonproliferative diabetic retinopathy OU. Systemic history was remarkable for type II diabetes mellitus (for 7
years), hypertension, and a previous cerebral vascular
accident, for which the patient showed a left homonymous superior quadrantanopia (see Figures 2A and B).
Patient C was taking lisinopril, amlodipine besylate,
clopidogrel, propranolol, metformin, and aspirin for his
systemic conditions. Best-corrected visual acuities at
distance were 20/40 O.D. and 20/30 O.S. Pupils and
ocular motilities were within normal limits. Slit lamp
examination was unremarkable, and intraocular pressures
were 18 mmHg OU. Dilated fundus examination found
an inferior ischemic retina O.D. with a plaque at the
bifurcation of the retinal arteriolar tree O.D. No carotid
bruit was heard on the left or right side. The patient was
referred for an immediate carotid workup, which included a carotid duplex examination, magnetic resonance
angiography (MRA) of the neck (see Figure 3), and a
magnetic resonance image (MRI) of the head. Automated
threshold visual fields were also completed. Results of
carotid studies showed calcified atherosclerotic plaques
present at the level of the common carotid artery with
50% to 79% stenosis of the right internal carotid artery

84

Figure 2

Optometry, Vol 77, No 2, February 2006

Automated threshold visual fields for Patient C.

Trego and Pagani

Figure 3

Clinical Care

MRA shows stenosis of the internal carotid artery.

with no stenosis of the left internal carotid. MRI studies
showed a right cerebral peduncle (brainstem) infarct.
Visual fields showed a superior altitudinal field loss O.D.
(see Figures 2C and D) compared with the previous
visual fields, which showed a left homonymous superior
quadranopsia (see Figures 2A and B). The patient is
being followed up by a vascular specialist and is being
monitored closely for ocular complications of carotid
artery disease.

Discussion
A variety of transient visual signs or symptoms may develop in patients with disease of the carotid arteries. Ultimately, the hallmark of these disturbances is their monocular nature, ipsilateral to the carotid disease. Such ocular
signs and symptoms include transient monocular visual loss
(amaurosis fugax), venous stasis retinopathy or ocular ischemic syndrome, central retinal artery occlusion, ischemic
optic neuropathy, Horner’s syndrome, and oculomotor
nerve palsy.2-4 A recent study performed by McCullough et
al.,8 found that the predictive value of ocular fundoscopic
findings for identifying carotid artery occlusive disease is
variable but generally poor. Ocular findings of moderate
predictive values that warranted further diagnostic testing
included retinal emboli, venous stasis retinopathy, and amaurosis fugax. Other ocular findings with poor prediction of
carotid occlusive disease included ischemic optic neuropathy, retinal artery or vein occlusion, asymmetric diabetic
retinopathy, optic atrophy, and ocular ischemic syndrome.8
Yet, of all presenting symptoms, transient monocular vision
loss (TMVL) is the most universal and perhaps the most
important ophthalmic symptom of carotid occlusive disease.1 Patients with TMVL typically complain of acute,

85
monocular loss of vision that may be partial or incomplete.
In the North American Symptomatic Carotid Endarterectomy Trial (NASCET), 53.4% of 554 patients reported
sudden, painless, and diffuse loss of vision and altitudinal
visual loss with a descending or ascending shade reported in
28.8% of patients.1,4 Most episodes of TMVL last 2 to 30
minutes and then resolve spontaneously, usually over seconds and minutes. Lesions of the common or internal
carotids often cause this TMVL, secondary to emboli within
the retinal circulation. With emboli, most commonly a black
or dark shade spreads across the visual field of the affected
eye, disappearing after a few seconds or minutes at most.
Less commonly, severe stenosis of the carotid artery causes
TMVL secondary to retinal or choroidal hypoperfusion.1
All 3 patients presented with some form of monocular
vision loss. Patient A presented with blurring of vision upon
extreme left head turn, Patient B presented with a “black
spot” over her right eye, and Patient C noted the inability to
see the upper half of his visual field in the right eye.
Although all 3 were different in presenting symptoms, all
reported the visual loss ipsilateral to the stenosed carotid
artery.
In addition to the presenting symptom of monocular
vision loss ipsilateral to the stenosed carotid, which is
significant clinical evidence for carotid occlusive disease,
all 3 patients exhibited retinal emboli in their arteriolar
trees. Common locations for emboli include the origins of
the major arteries such as the internal carotid artery, middle
cerebral artery, basilar artery, vertebral arteries, and aortic
arch (see Figure 4). Emboli, often asymptomatic, may
consist of calcium from a diseased heart valve, organisms,
or foreign materials such as talc, fat, or tumor cells and
cholesterol.5 The presence of retinal emboli carries implications for the patient’s future health status and is often
associated with systemic vascular disease (see Table). Results of the Beaver Dam Eye Study showed that the overall
prevalence of retinal emboli in a population of 4,926 patients was 1.3%, increasing to 3.1% in patients 75 years or
older.5,6 Researchers of this study also found an increase in
stroke and cardiac-related deaths among those patients with
retinal emboli. This study supports the notion that patients
with retinal emboli are more systemically ill than patients
without emboli.6 In addition to plaques at the bifurcation of
their arteriolar trees, all 3 patients also exhibited systemic
vascular diseases often associated with retinal emboli, in-

Table Concomitant medical conditions associated with
retinal arterial emboli29
Systemic vascular disease

Incidence of concurrence with
retinal arterial emboli (%)

Hypertension
Diabetes mellitus
Cardiac disease
Elevated cholesterol levels
Carotid stenosis ipsilateral

70.0
45.0
41.0
59.0
55.2

86

Figure 4 Diagram of blood flow from the carotid system. (Reprinted
from www.meddean.luc.edu/lumen/MedEd/Neuro/neurovasc/navigation/
ica.htm with permission from Loyola University Medical Education (LUMEN)
and Christopher Ladner, M.D., Ph.D.

cluding hypertension, diabetes mellitus, and high cholesterol.
As primary eye care providers, we play a pivotal role in
the recommended followup and referral of these “at risk”
patients. Patients suspected of having carotid artery disease
require prompt, noninvasive vascular evaluation to confirm
the carotid lesion, establish its cause (atheroma, dissection,
vasculitis, compression), and assess the severity of the
lesion (percentage of occlusion/stenosis) and its ocular and
cerebral tolerance (hypoperfusion of the ipsilateral eye and
hemisphere).1,3 Oculoplethysmography (OPG) is a wellknown noninvasive test used to detect the presence of
blockage in the carotid arteries by changes in flow and
pressure from the hemodynamically significant lesions.9
OPG can be used as an initial semiquantitative measurement
in the estimation of blockage in the carotid arteries and their
tributaries in symptomatic or asymptomatic patients with
bruits.9,10 However, clinical evidence has shown that OPG
is not a reliable screening test for carotid artery disease,
particularly in nonocclusive unilateral disease or bilateral
disease.11 A recent study examined the use of pulsatile
ocular blood flow (POBF) as a noninvasive technique to
examine severe stenosis of the internal carotid artery.12
POBF repeatedly measures intraocular pressure with a
pneumatic applanation tonometer during the cardiac pulse
cycle and, based on intraocular pressure variation with time,
calculates the pulsatile ocular blood flow.13 Although not a
direct reflection of blood flow of the internal carotid artery,
low or unrecordable POBF may signify severe stenosis and
alert the primary eye care provider that further investigation
is needed.12
Carotid duplex ultrasonography is the singular noninvasive diagnostic tool for the evaluation of extracranial
carotid disease. Carotid duplex scanning can accurately
measure the degree of extracranial carotid artery stenosis

Optometry, Vol 77, No 2, February 2006
and can provide important information about the vessel
wall configuration and plaque morphology.1,14-18 In addition to carotid duplex ultrasonography, MRA can also
be a diagnostic tool in screening for carotid arteriosclerosis and evaluating intracranial hemodynamics. MRA is
not as efficient as a carotid duplex in the analysis of
plaque morphology, in the estimation of stenosis, and in
carotid interpretation.16,17,19 Although an MRA is diagnostic, it carries a higher morbidity and mortality rate
than ultrasonography.2 However, by combining the carotid Doppler with the MRA, the information obtained on
carotid artery disease morphology is revealing. All 3
patients underwent carotid duplex testing, which revealed
the stenosis of their respective internal carotid arteries. In
addition, Patient C also underwent an MRA, to further
support the diagnosis.
Two major prospective studies, North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the
European Carotid Surgery Trial (ECST) provide strong
evidence for the benefit of carotid endarterectomy in symptomatic patients when performed by experienced surgeons.1,5,15,20-21 Both studies showed that in patients with
retinal or hemispheric symptoms attributed to severe (70%
to 99%) carotid stenosis, endarterectomy was superior to
medical care alone. There was no benefit of carotid endarterectomy in symptomatic patients with mild stenosis
(⬍50%).5,20-21 Patients with carotid artery disease, who are
asymptomatic, are prevalent in the general population.
However severe (⬎70%) carotid stenosis of the asymptomatic patient is rare in comparison with symptomatic patients.
Four randomized clinical trials were conducted (Carotid
Artery Surgery Asymptomatic Narrowing Operation Versus
Aspirin [CASANOVA], Mayo Asymptomatic Carotid Endarterectomy [MACE] Trial, Veterans Affairs Asymptomatic
Carotid Endarterectomy Trial, and the Asymptomatic Carotid Atherosclerosis Study [ACAS]) to determine the risks
and benefits of carotid endarterectomy in asymptomatic
patients. CASANOVA, MACE, and the Veteran Affairs
Asymptomatic Trial found no benefit from surgery in
asymptomatic patients.5,15,22-27 Based on a 5-year projection, the ACAS found that carotid endarterectomy reduced
the risk of absolute stroke by 5.9% and the relative risk of
stroke and death by 53%. Patients enrolled in ACAS were
younger than 80 years and had asymptomatic carotid stenosis of 60% or more.15,26 The overall benefit of endarterectomy strongly depends on surgical risk. Mortality and morbidity rates associated with carotid endarterectomy are
significantly lower in asymptomatic patients than in symptomatic patients.15,25-27
Because all 3 patients chose not to undergo carotid
endartectomy, optometric management should include a
dilated fundus examination every 6 months, monitoring
closely for ocular complications of carotid artery disease
and ocular ischemic syndrome. In addition to careful
ocular examination, comanagement with their primary
provider and a vascular specialist is recommended.

Trego and Pagani

Clinical Care

Conclusion
These 3 presentations show that through proper management of patients over 50 who present with chief complaints
of monocular vision loss, a differential diagnosis of carotid
artery disease should be considered. Patients who exhibit
retinal arterial emboli are at an increased risk for both stroke
and vascular death. Appropriate measures for confirming a
diagnosis include carotid duplex ultrasound imaging, MRA,
and carotid angioplasty. Proper management of these patients includes a dilated fundus examination every 6 months
and monitoring closely for ocular complications of carotid
artery disease. Further medical management with antiplatelet therapy, risk factor modification, as well as surgical
techniques such as carotid angioplasty and carotid endarterectomy may be recommended.28

References
1. Biousse V. Carotid disease and the eye. Curr Opin Ophthalmol
1997;8:16-26.
2. Alexander LJ. Variations in physicians response to consultation requests for Hollenhorst plaques: a pilot study. J Am Optom Assoc
1992;63(5):326-32.
3. American Heart Association Medical/Scientific Statement. Guidelines
for the management of patients with transient ischemic attacks. Stroke
1994;25:1320-35.
4. Streifler JY, Eliaziw M, Benavente OR, et al, for the North American
Symptomatic Carotid Endarterectomy Trial. The risk of stroke with
first-ever retinal vs hemispheric transient ischemic attacks and high
grade stenosis. Arch Neurol 1995;52:246-9.
5. Egan RA, Biousse V. Update on ischemic stroke. Curr Opin Ophthalmol 2000; 11:395-402.
6. Klein R, Klein BEK, Jensen SC, et al. Retinal emboli and stroke: The
Beaver Eye Dam Study. Arch Ophthalmol 1999;117:1063-8.
7. Recchia FM, Brown GC. Systemic disorders associated with retinal
vascular occlusion. Curr Opin Ophthalmol 2000;11:462-7.
8. McCullough HK, Reinert CG, Hynan LS, et al. Ocular findings as
predictors or carotid occlusive disease: is carotid imaging justified? J
Vasc Surg 2004;40:279-86.
9. Wasserman DH, Hobson RW, Lynch TG, et al. Ultrasonic imaging and
oculoplethysmography in diagnosis of carotid occlusive disease. Arch
Surg 1983;118:1161-3.
10. Graham AA. Plethysmography: safety, effectiveness, and clinical
utility in diagnosing vascular disease. Health Technol Assess (Rockv)
1996;7:1-46.
11. Blakeley DD, Oddone EZ, Hasselblad V, et al. Noninvasive carotid
artery testing: a meta-analytic review. Ann Intern Med 1995;122:
360-7.

87
12. Barkana Y, Harris A, Hefez L, et al. Unrecordable pulsatile ocular
blood flow may signify severe stenosis of the ipsilateral internal
carotid artery. Br J Ophthalmol 2005;87:1478-80.
13. Silver DM, Farrell RA. Validity of pulsatile ocular blood flow measurements. Surv Ophthalmol 1994;38:S72-80.
14. Sharma S, Brown GC, Pater JL, et al. Does a visible retinal embolus
increase the likelihood of hemodynamically significant carotid artery
stenosis in patients with acute retinal arterial occlusion? Arch Ophthalmol 1998;116:1602-6.
15. Biller J, Thies W. When to operate in carotid artery disease. Am Fam
Physician 2000; 61:400-6.
16. Garcia JH, Khang-Loon H. Carotid atherosclerosis: definition, pathogenesis, and clinical significance. Neuroimaging Clin North Am 1996;
6:801-10.
17. El-Barghouty N, Nicolaides A, Bahal V, et al. The identification of
the high risk carotid plaque. Eur J Vasc Endovasc Surg 1996;11:
470-8.
18. Hatsukami TS, Ferguson MS, Beach KW, et al. Carotid plaque
morphology and clinical events. Stroke 1997; 28:95-100.
19. Golinik KC, Hund PW, Stroman GA, et al. Magnetic resonance
imaging in patients with unexplained optic neuropathy. Ophthalmology 1996;103:515-20.
20. North American Symptomatic Carotid Endarterectomy Trial
(NASCET) Collaborators. Beneficial effect of carotid endarterectomy
in symptomatic patients with high-grade carotid stenosis. N Engl
J Med 1991;325:445-53.
21. European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients
with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet
1991;337:1235-43.
22. Norris JW, Zhu CA, Bornstein NM, et al. Vascular risks of asymptomatic carotid stenosis. Stroke 1991;22:1485-90.
23. CASANOVA Study Group. Carotid surgery versus medical therapy in
asymptomatic carotid stenosis. Stroke 1991;22:1229-35.
24. Mayo Asymptomatic Carotid Endarterectomy Study Group. Results of
a randomized controlled trial of carotid Endarterectomy for asymptomatic carotid stenosis. Mayo Clin Proc 1992;67:513-8.
25. Hobson RW 2nd, Weiss DG, Fields WS, et al. Efficacy of carotid
endarterectomy for asymptomatic carotid stenosis. N Engl J Med
1993;328:276-9.
26. Executive Committee for the Asymptomatic Carotid Atherosclerosis
Study. Endarterectomy for asymptomatic carotid stenosis. JAMA
1995;273:1421-8.
27. European Carotid Surgery Trialists’ Collaborative Group. Risk of
stroke in the distribution of an asymptomatic carotid artery. Lancet
1995;345:209-12.
28. Wijman C, Gomes JA, Winter MR, et al. Symptomatic and asymptomatic retinal embolism have different mechanisms. Stroke 2004;35:
e100-2.
29. Schwarcz TH, Eton D, Ellenby MI, et al. Hollenhorst plaques: Retinal
manifestations and the role of carotid endarterectomy. J Vasc Surg
1990;11:635-41.