- Email: [email protected]
Light-Induced Amaurosis—A Case Report and Brief Literature Review
Journal Pre-proof Light-induced amaurosis – a case report and brief literature review. Jason Tsai, Bala Ramanan, MBBS, J. Gregory Modrall, MD, Paul W. Hurd, Shirling Tsai, MD PII:
S0890-5096(20)30152-7
DOI:
https://doi.org/10.1016/j.avsg.2020.01.096
Reference:
AVSG 4898
To appear in:
Annals of Vascular Surgery
Received Date: 6 November 2019 Revised Date:
14 January 2020
Accepted Date: 15 January 2020
Please cite this article as: Tsai J, Ramanan B, Modrall JG, Hurd PW, Tsai S, Light-induced amaurosis – a case report and brief literature review., Annals of Vascular Surgery (2020), doi: https://doi.org/10.1016/ j.avsg.2020.01.096. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2020 Published by Elsevier Inc.
Title: Light-induced amaurosis – a case report and brief literature review.
Authors: Jason Tsai1; Bala Ramanan,1,2 MBBS; J. Gregory Modrall1,2 MD, Paul W. Hurd1,3, Shirling Tsai1,2 MD
1. Dallas Veterans Affairs Medical Center, 4500 South Lancaster Road, Dallas TX 75216. 2. Department of Surgery, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas TX 75390. 3. Department of Neurology & Neurotherapeutics, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas TX 75390.
Corresponding author: Shirling Tsai, MD Surgical Services Dallas VA Medical Center 4500 South Lancaster Road Dallas TX 75216 [email protected]
This material is the result of work supported with resources and the use of facilities at the VA North Texas Health Care Systems. The contents do not represent the views of the U.S. Department of Veterans Affairs or the United States Government.
1 1
Abstract
2
Light induced amaurosis is a rare manifestation of symptomatic carotid artery disease. Unlike
3
amaurosis fugax, which is often attributed to embolic phenomenon associated with carotid artery
4
disease, light induced amaurosis has been associated with reduced perfusion to the eye,
5
secondary to carotid artery disease, leading to retinal ischemia. The case described here is that of
6
a 67-year-old male with bilateral vision loss in response to bright light. Imaging revealed severe
7
internal carotid stenosis on the right and occlusion of the internal carotid artery on the left.
8
Similar to previous cases reported in the literature, the symptoms resolved after carotid
9
endarterectomy.
10 11
Introduction
12
Although amaurosis fugax is commonly characterized by transient darkening of the
13
visual field, there exists a rarer form of transient visual deficit commonly characterized by
14
unilateral loss of vision in response to bright light exposure. Unlike amaurosis fugax, which is
15
often attributed to embolic phenomenon associated with carotid disease, light induced amaurosis
16
(LIA) is considered a hemodynamic phenomenon. Its identifiable cause is usually severe carotid
17
artery disease, leading to retinal ischemia.
18 19 20
Case Report The patient is a 67 – year-old white male who presented with bilateral impairment of
21
vision upon exposure to bright light in the setting of a chronic left carotid occlusion and a severe
22
right carotid artery stenosis. Symptoms had been occurring for the past 2-3 months. He stated
23
that he had episodes in which his vision in both eyes "whites out" for 3-4 minutes at a time when
2 24
gazing into bright lights, such a computer or television screen, and headlights from oncoming
25
traffic while driving at night. The incidents of vision loss had no other inciting events and
26
resolved spontaneously. There was no associated nausea, vomiting, numbness, slurring of
27
speech, weakness, headache, or pain. The patient had a history of diabetes and hypertension, but
28
no significant cardiac history, previous stroke, or TIA. An ophthalmology evaluation concluded
29
there was no evidence of ocular pathology to explain the symptoms and recommended a
30
neurology evaluation. By the time the patient was referred to neurology, his visual symptoms
31
had progressed and were occurring twice a week. He described his symptoms as bilateral
32
whitening of vision when staring at bright lights, starting from the center of his visual field and
33
expanding outwards. He noted that he retained some peripheral visual ability. An MRI and CT
34
angiogram of the head and neck were performed. The MRI revealed an acute lacunar infarct in
35
the right frontal lobe and multiple non-specific T2/FLAIR hyperintensities in the periventricular
36
and deep white matter. There was also evidence of a remote lacunar infarct in the left centrum
37
semiovale. CTA revealed a 70% focal stenosis of the right internal carotid artery (ICA), based
38
on centerline measurements and NASCET criteria for calculating ICA stenosis (Figure 1).
39
Imaging of the Circle of Willis was notable for a severe stenosis in the P1 segment of the left
40
posterior cerebral artery with a patent posterior communicating artery on the left. The remainder
41
of the intracranial circulation was normal. Specifically, on the right, the anterior, middle, and
42
posterior cerebral arteries were patent without significant stenosis. On the left, the intracranial
43
ICA reconstituted in the supraclinoid portion and the left anterior and middle arteries were
44
patent. Bilateral vertebral arteries were patent, and duplex confirmed antegrade flow in bilateral
45
vertebral arteries.
3 46
The case was discussed with our neurology colleagues. None of the infarcts seen on MRI
47
provided an adequate explanation of the patient’s visual deficits. Additionally, his symptoms
48
were not consistent with classic amaurosis fugax, typically associated with transient darkening of
49
the vision in one eye. The combination of severe ICA stenosis with contralateral ICA occlusion
50
suggested that his visual symptoms may indicate compromised perfusion either to the brain or
51
the eye, rather than an embolic event. Furthermore, the patient’s unique complaint of “whitening
52
out” of his vision in response to bright lights was suggestive of retinal artery ischemia, as seen in
53
light-induced amaurosis. Therefore, right carotid endarterectomy was recommended and
54
performed. One month later, in a follow-up visit to ophthalmology, the patient reported no
55
further visual symptoms, with no loss in visual acuity, and it was concluded that the amaurosis
56
was resolved. Follow-up one year later with carotid duplex revealed a widely patent right
57
internal carotid artery, and no return of visual symptoms. It was determined that successful
58
revascularization of the carotid artery led to complete and immediate resolution of bilateral LIA
59
symptoms without reoccurrence.
60 61 62
Discussion This case of light induced amaurosis followed a unique presentation, specifically bilateral
63
visual symptoms precipitated by exposure to bright light. The etiology of these symptoms was
64
suspected to be bilateral carotid artery disease, causing retinal ischemia. This is unusual because
65
bilateral ocular symptoms are commonly associated with deficits in the central nervous system
66
(brain) whereas unilateral symptoms often stem from deficits in the eye or retina. However, in
67
this patient with a left ICA occlusion and right ICA stenosis, perfusion in the left eye was
68
dependent upon collaterals from the right; therefore, both eyes may be susceptible to ischemia
69
secondary to the right sided carotid disease.
4 70
In cases of loss of vision, the nature of the symptoms often gives clues to the location of
71
the lesion due to the retinotopic organization of the visual pathway. Injury or infarcts in the
72
retina or optic nerve result in monocular vision loss in the ipsilateral eye. Damage to the primary
73
visual cortices, such as an occipital lobe infarct, results in contralateral loss of vision. Some
74
cases of severe posterior circulation stroke can result in binocular vision loss, however in those
75
cases, symptoms often include homonymous hemianopia, vertigo, imbalance, and sensory
76
deficits.1 These CNS lesions can mimic the symptoms of bilateral amaurosis fugax and were
77
considered as differential diagnoses.
78
There have been a handful of previous reports of LIA in the literature.2-6 In a series of 5
79
patients with unilateral vision loss in response to bright light, Furlan et al found reduced
80
ipsilateral retinal artery pressure and occlusion or high-grade stenosis of the ipsilateral internal
81
carotid.2 A subsequent series of 4 patients with LIA also documented macular region ischemia
82
associated with episodes of vision loss.3 The carotid disease was hypothesized to reduce
83
perfusion to the flow threshold of electrical failure, which caused the visual blurring effects upon
84
exposure to bright light. Thus, retinal ischemia would result in an inadequate regeneration of
85
retinal pigments after light bleaching.3
86
Wiebers and colleagues described a series of four cases of bilateral loss of vision in
87
response to bright light.4 Each patient had angiographically documented bilateral high-grade
88
stenosis of the internal carotid arteries. Two of these patients went on to undergo carotid
89
endarterectomy, while the other two were treated with aspirin. Symptoms for patients who
90
underwent surgery either improved significantly or resolved during follow-up. The two patients
91
treated with aspirin continued to be symptomatic and one patient died of an acute myocardial
92
infarction three months after the assessment. The symptoms of these patients were noted to differ
5 93
from bilateral occipital lobe ischemia caused by vertebrobasilar system disease. Although the
94
visual deficit associated with occipital lobe ischemia is often bilateral in nature, it often involves
95
combinations of right or left hemianopsias with or without sparing of central vision. Most
96
importantly, it is not related to exposure to bright light, and patients often have other symptoms
97
of vertebrobasilar insufficiency. Through this study, Wiebers identified a critical distinction of
98
light induced amaurosis as a manifestation of carotid artery disease rather than vertebral-basilar
99
insufficiency.4
100
Kaiboriboon also described a patient with symptoms consistent with light induced
101
amaurosis. The visual loss occurred unilaterally, but then later spread to the other eye. The left
102
internal carotid artery was completely occluded and the right internal carotid and both external
103
carotids were severely stenosed. After a right carotid endarterectomy, the patient’s symptoms
104
resolved, and visual function was restored without reoccurrence. This case most closely
105
resembles our patient, in that chronic occlusion of one internal carotid artery with severe stenosis
106
of the contralateral side can cause bilateral symptoms of light-induced amaurosis.5
107
The diagnosis of light-induced amaurosis may be challenging and is often made after
108
other more common diagnoses are ruled out. Since the ischemic event is believed to be
109
secondary to inadequate perfusion, it is possible that perfusion imaging may aid in diagnosis.
110
However, in our literature search, we did not find any reports of use of transcranial Doppler or
111
perfusion imaging. Only one report of two patients assessed flow in the ophthalmic artery, and
112
in this case report, visual symptoms were associated with direction of flow in the ophthalmic
113
artery.7 Furthermore, although there appears to be inadequate perfusion to the retina, there are
114
no reports of an associated global cerebral hypoperfusion. However, in some reported cases,
6 115
visual symptoms occurred in response to bright light or in response to rapid changes in position
116
or standing up, which would be consistent with a state of borderline perfusion.2
117
Management of patients with light-induced amaurosis has also varied in the literature.
118
Unfortunately, our understanding of the natural history of light-induced amaurosis is limited to a
119
handful of case reports. In a report of five patients with light-induced amaurosis, three were
120
managed medically with follow-up of 2.5, 4, and 7 years.2 Each of these patients had persistent
121
visual symptoms, but there were no reports of subsequent stroke or TIA. In this respect, light-
122
induced amaurosis appears to have a more benign natural history than other TIA or stroke.
123
However, the number of case reports is small, so the true natural history remains unknown.
124
Even less well defined are indications for surgery in patients with light-induced amaurosis. In
125
two cases, patients had light-induced amaurosis in one eye and known severe ipsilateral ICA
126
stenosis and contralateral upper extremity weakness or tingling.2,5 After CEA, which in one case
127
was driven by the contralateral upper extremity symptoms, the eye symptoms resolved. The
128
literature supports the conclusion that patients with light-induced amaurosis respond well to
129
carotid endarterectomy, however there is little data informing us of the risk of subsequent stroke
130
or TIA in patients with untreated light-induced amaurosis.
131 132 133
Conclusion Light induced amaurosis is a rare hemodynamic manifestation of carotid artery disease.6
134
These episodes of visual loss are brief and occur when looking at sources of bright light. The
135
symptoms reflect episodes of transient retinal ischemia associated with carotid artery disease,
136
which can be corrected with carotid endarterectomy.
137
7 138 139
Author Contributions:
140
JT: Initial manuscript preparation and literature review
141
BR: Manuscript editing
142
JGM: Manuscript editing
143
PWH: Manuscript editing
144
ST: Initial manuscript preparation, literature review and editing
145
8 146
Figure Legend
147 148
Figure 1. CT angiogram with 3-dimensional reconstruction (A) and maximum intensity projection (MIP) view (B) showing severe right ICA stenosis and occlusion of the left ICA.
9 149
References
150 151 152 153 154 155 156 157 158 159 160 161 162 163
1. 2.
164
3. 4. 5. 6.
7.
Merwick A, Werring D. Posterior circulation ischaemic stroke. Bmj. 2014;348:g3175. Furlan AJ, Whisnant JP, Kearns TP. Unilateral visual loss in bright light. An unusual symptom of carotid artery occlusive disease. Arch Neurol. 1979;36(11):675-676. Donnan GA, Sharbrough FW, Whisnant JP. Carotid occlusive disease. Effect of bright light on visual evoked response. Arch Neurol. 1982;39(11):687-689. Wiebers DO, Swanson JW, Cascino TL, Whisnant JP. Bilateral loss of vision in bright light. Stroke; a journal of cerebral circulation. 1989;20(4):554-558. Kaiboriboon K, Piriyawat P, Selhorst JB. Light-induced amaurosis fugax. Am J Ophthalmol. 2001;131(5):674-676. Brigham RA, Youkey JR, Clagett GP, et al. Bright-light amaurosis fugax: an unusual symptom of retinal hypoperfusion corrected by external carotid revascularization. Surgery. 1985;97(3):363368. Giroud M, Gras P, Dumas R, Becker F. Bilateral loss of vision in bright light. Stroke; a journal of cerebral circulation. 1991;22(3):415-416.
S0890-5096(20)30152-7
DOI:
https://doi.org/10.1016/j.avsg.2020.01.096
Reference:
AVSG 4898
To appear in:
Annals of Vascular Surgery
Received Date: 6 November 2019 Revised Date:
14 January 2020
Accepted Date: 15 January 2020
Please cite this article as: Tsai J, Ramanan B, Modrall JG, Hurd PW, Tsai S, Light-induced amaurosis – a case report and brief literature review., Annals of Vascular Surgery (2020), doi: https://doi.org/10.1016/ j.avsg.2020.01.096. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2020 Published by Elsevier Inc.
Title: Light-induced amaurosis – a case report and brief literature review.
Authors: Jason Tsai1; Bala Ramanan,1,2 MBBS; J. Gregory Modrall1,2 MD, Paul W. Hurd1,3, Shirling Tsai1,2 MD
1. Dallas Veterans Affairs Medical Center, 4500 South Lancaster Road, Dallas TX 75216. 2. Department of Surgery, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas TX 75390. 3. Department of Neurology & Neurotherapeutics, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas TX 75390.
Corresponding author: Shirling Tsai, MD Surgical Services Dallas VA Medical Center 4500 South Lancaster Road Dallas TX 75216 [email protected]
This material is the result of work supported with resources and the use of facilities at the VA North Texas Health Care Systems. The contents do not represent the views of the U.S. Department of Veterans Affairs or the United States Government.
1 1
Abstract
2
Light induced amaurosis is a rare manifestation of symptomatic carotid artery disease. Unlike
3
amaurosis fugax, which is often attributed to embolic phenomenon associated with carotid artery
4
disease, light induced amaurosis has been associated with reduced perfusion to the eye,
5
secondary to carotid artery disease, leading to retinal ischemia. The case described here is that of
6
a 67-year-old male with bilateral vision loss in response to bright light. Imaging revealed severe
7
internal carotid stenosis on the right and occlusion of the internal carotid artery on the left.
8
Similar to previous cases reported in the literature, the symptoms resolved after carotid
9
endarterectomy.
10 11
Introduction
12
Although amaurosis fugax is commonly characterized by transient darkening of the
13
visual field, there exists a rarer form of transient visual deficit commonly characterized by
14
unilateral loss of vision in response to bright light exposure. Unlike amaurosis fugax, which is
15
often attributed to embolic phenomenon associated with carotid disease, light induced amaurosis
16
(LIA) is considered a hemodynamic phenomenon. Its identifiable cause is usually severe carotid
17
artery disease, leading to retinal ischemia.
18 19 20
Case Report The patient is a 67 – year-old white male who presented with bilateral impairment of
21
vision upon exposure to bright light in the setting of a chronic left carotid occlusion and a severe
22
right carotid artery stenosis. Symptoms had been occurring for the past 2-3 months. He stated
23
that he had episodes in which his vision in both eyes "whites out" for 3-4 minutes at a time when
2 24
gazing into bright lights, such a computer or television screen, and headlights from oncoming
25
traffic while driving at night. The incidents of vision loss had no other inciting events and
26
resolved spontaneously. There was no associated nausea, vomiting, numbness, slurring of
27
speech, weakness, headache, or pain. The patient had a history of diabetes and hypertension, but
28
no significant cardiac history, previous stroke, or TIA. An ophthalmology evaluation concluded
29
there was no evidence of ocular pathology to explain the symptoms and recommended a
30
neurology evaluation. By the time the patient was referred to neurology, his visual symptoms
31
had progressed and were occurring twice a week. He described his symptoms as bilateral
32
whitening of vision when staring at bright lights, starting from the center of his visual field and
33
expanding outwards. He noted that he retained some peripheral visual ability. An MRI and CT
34
angiogram of the head and neck were performed. The MRI revealed an acute lacunar infarct in
35
the right frontal lobe and multiple non-specific T2/FLAIR hyperintensities in the periventricular
36
and deep white matter. There was also evidence of a remote lacunar infarct in the left centrum
37
semiovale. CTA revealed a 70% focal stenosis of the right internal carotid artery (ICA), based
38
on centerline measurements and NASCET criteria for calculating ICA stenosis (Figure 1).
39
Imaging of the Circle of Willis was notable for a severe stenosis in the P1 segment of the left
40
posterior cerebral artery with a patent posterior communicating artery on the left. The remainder
41
of the intracranial circulation was normal. Specifically, on the right, the anterior, middle, and
42
posterior cerebral arteries were patent without significant stenosis. On the left, the intracranial
43
ICA reconstituted in the supraclinoid portion and the left anterior and middle arteries were
44
patent. Bilateral vertebral arteries were patent, and duplex confirmed antegrade flow in bilateral
45
vertebral arteries.
3 46
The case was discussed with our neurology colleagues. None of the infarcts seen on MRI
47
provided an adequate explanation of the patient’s visual deficits. Additionally, his symptoms
48
were not consistent with classic amaurosis fugax, typically associated with transient darkening of
49
the vision in one eye. The combination of severe ICA stenosis with contralateral ICA occlusion
50
suggested that his visual symptoms may indicate compromised perfusion either to the brain or
51
the eye, rather than an embolic event. Furthermore, the patient’s unique complaint of “whitening
52
out” of his vision in response to bright lights was suggestive of retinal artery ischemia, as seen in
53
light-induced amaurosis. Therefore, right carotid endarterectomy was recommended and
54
performed. One month later, in a follow-up visit to ophthalmology, the patient reported no
55
further visual symptoms, with no loss in visual acuity, and it was concluded that the amaurosis
56
was resolved. Follow-up one year later with carotid duplex revealed a widely patent right
57
internal carotid artery, and no return of visual symptoms. It was determined that successful
58
revascularization of the carotid artery led to complete and immediate resolution of bilateral LIA
59
symptoms without reoccurrence.
60 61 62
Discussion This case of light induced amaurosis followed a unique presentation, specifically bilateral
63
visual symptoms precipitated by exposure to bright light. The etiology of these symptoms was
64
suspected to be bilateral carotid artery disease, causing retinal ischemia. This is unusual because
65
bilateral ocular symptoms are commonly associated with deficits in the central nervous system
66
(brain) whereas unilateral symptoms often stem from deficits in the eye or retina. However, in
67
this patient with a left ICA occlusion and right ICA stenosis, perfusion in the left eye was
68
dependent upon collaterals from the right; therefore, both eyes may be susceptible to ischemia
69
secondary to the right sided carotid disease.
4 70
In cases of loss of vision, the nature of the symptoms often gives clues to the location of
71
the lesion due to the retinotopic organization of the visual pathway. Injury or infarcts in the
72
retina or optic nerve result in monocular vision loss in the ipsilateral eye. Damage to the primary
73
visual cortices, such as an occipital lobe infarct, results in contralateral loss of vision. Some
74
cases of severe posterior circulation stroke can result in binocular vision loss, however in those
75
cases, symptoms often include homonymous hemianopia, vertigo, imbalance, and sensory
76
deficits.1 These CNS lesions can mimic the symptoms of bilateral amaurosis fugax and were
77
considered as differential diagnoses.
78
There have been a handful of previous reports of LIA in the literature.2-6 In a series of 5
79
patients with unilateral vision loss in response to bright light, Furlan et al found reduced
80
ipsilateral retinal artery pressure and occlusion or high-grade stenosis of the ipsilateral internal
81
carotid.2 A subsequent series of 4 patients with LIA also documented macular region ischemia
82
associated with episodes of vision loss.3 The carotid disease was hypothesized to reduce
83
perfusion to the flow threshold of electrical failure, which caused the visual blurring effects upon
84
exposure to bright light. Thus, retinal ischemia would result in an inadequate regeneration of
85
retinal pigments after light bleaching.3
86
Wiebers and colleagues described a series of four cases of bilateral loss of vision in
87
response to bright light.4 Each patient had angiographically documented bilateral high-grade
88
stenosis of the internal carotid arteries. Two of these patients went on to undergo carotid
89
endarterectomy, while the other two were treated with aspirin. Symptoms for patients who
90
underwent surgery either improved significantly or resolved during follow-up. The two patients
91
treated with aspirin continued to be symptomatic and one patient died of an acute myocardial
92
infarction three months after the assessment. The symptoms of these patients were noted to differ
5 93
from bilateral occipital lobe ischemia caused by vertebrobasilar system disease. Although the
94
visual deficit associated with occipital lobe ischemia is often bilateral in nature, it often involves
95
combinations of right or left hemianopsias with or without sparing of central vision. Most
96
importantly, it is not related to exposure to bright light, and patients often have other symptoms
97
of vertebrobasilar insufficiency. Through this study, Wiebers identified a critical distinction of
98
light induced amaurosis as a manifestation of carotid artery disease rather than vertebral-basilar
99
insufficiency.4
100
Kaiboriboon also described a patient with symptoms consistent with light induced
101
amaurosis. The visual loss occurred unilaterally, but then later spread to the other eye. The left
102
internal carotid artery was completely occluded and the right internal carotid and both external
103
carotids were severely stenosed. After a right carotid endarterectomy, the patient’s symptoms
104
resolved, and visual function was restored without reoccurrence. This case most closely
105
resembles our patient, in that chronic occlusion of one internal carotid artery with severe stenosis
106
of the contralateral side can cause bilateral symptoms of light-induced amaurosis.5
107
The diagnosis of light-induced amaurosis may be challenging and is often made after
108
other more common diagnoses are ruled out. Since the ischemic event is believed to be
109
secondary to inadequate perfusion, it is possible that perfusion imaging may aid in diagnosis.
110
However, in our literature search, we did not find any reports of use of transcranial Doppler or
111
perfusion imaging. Only one report of two patients assessed flow in the ophthalmic artery, and
112
in this case report, visual symptoms were associated with direction of flow in the ophthalmic
113
artery.7 Furthermore, although there appears to be inadequate perfusion to the retina, there are
114
no reports of an associated global cerebral hypoperfusion. However, in some reported cases,
6 115
visual symptoms occurred in response to bright light or in response to rapid changes in position
116
or standing up, which would be consistent with a state of borderline perfusion.2
117
Management of patients with light-induced amaurosis has also varied in the literature.
118
Unfortunately, our understanding of the natural history of light-induced amaurosis is limited to a
119
handful of case reports. In a report of five patients with light-induced amaurosis, three were
120
managed medically with follow-up of 2.5, 4, and 7 years.2 Each of these patients had persistent
121
visual symptoms, but there were no reports of subsequent stroke or TIA. In this respect, light-
122
induced amaurosis appears to have a more benign natural history than other TIA or stroke.
123
However, the number of case reports is small, so the true natural history remains unknown.
124
Even less well defined are indications for surgery in patients with light-induced amaurosis. In
125
two cases, patients had light-induced amaurosis in one eye and known severe ipsilateral ICA
126
stenosis and contralateral upper extremity weakness or tingling.2,5 After CEA, which in one case
127
was driven by the contralateral upper extremity symptoms, the eye symptoms resolved. The
128
literature supports the conclusion that patients with light-induced amaurosis respond well to
129
carotid endarterectomy, however there is little data informing us of the risk of subsequent stroke
130
or TIA in patients with untreated light-induced amaurosis.
131 132 133
Conclusion Light induced amaurosis is a rare hemodynamic manifestation of carotid artery disease.6
134
These episodes of visual loss are brief and occur when looking at sources of bright light. The
135
symptoms reflect episodes of transient retinal ischemia associated with carotid artery disease,
136
which can be corrected with carotid endarterectomy.
137
7 138 139
Author Contributions:
140
JT: Initial manuscript preparation and literature review
141
BR: Manuscript editing
142
JGM: Manuscript editing
143
PWH: Manuscript editing
144
ST: Initial manuscript preparation, literature review and editing
145
8 146
Figure Legend
147 148
Figure 1. CT angiogram with 3-dimensional reconstruction (A) and maximum intensity projection (MIP) view (B) showing severe right ICA stenosis and occlusion of the left ICA.
9 149
References
150 151 152 153 154 155 156 157 158 159 160 161 162 163
1. 2.
164
3. 4. 5. 6.
7.
Merwick A, Werring D. Posterior circulation ischaemic stroke. Bmj. 2014;348:g3175. Furlan AJ, Whisnant JP, Kearns TP. Unilateral visual loss in bright light. An unusual symptom of carotid artery occlusive disease. Arch Neurol. 1979;36(11):675-676. Donnan GA, Sharbrough FW, Whisnant JP. Carotid occlusive disease. Effect of bright light on visual evoked response. Arch Neurol. 1982;39(11):687-689. Wiebers DO, Swanson JW, Cascino TL, Whisnant JP. Bilateral loss of vision in bright light. Stroke; a journal of cerebral circulation. 1989;20(4):554-558. Kaiboriboon K, Piriyawat P, Selhorst JB. Light-induced amaurosis fugax. Am J Ophthalmol. 2001;131(5):674-676. Brigham RA, Youkey JR, Clagett GP, et al. Bright-light amaurosis fugax: an unusual symptom of retinal hypoperfusion corrected by external carotid revascularization. Surgery. 1985;97(3):363368. Giroud M, Gras P, Dumas R, Becker F. Bilateral loss of vision in bright light. Stroke; a journal of cerebral circulation. 1991;22(3):415-416.