|
1
|
Ferreira BFA, Higashi AH, Prado LL, Gonçalves CR, Haddad MAO, Zacharias LC, Hirata CE, Yamamoto JH. OPTICAL COHERENCE TOMOGRAPHY ANGIOGRAPHY BIOMARKERS AND MICROPERIMETRY FEATURES IN BEHÇET'S UVEITIS. Retina 2023; 43:1680-1690. [PMID: 37531971 DOI: 10.1097/iae.0000000000003891] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/04/2023]
Abstract
PURPOSE To evaluate the parafoveal macular microvasculature and the macular function in patients with retinal vasculitis associated with Behçet's uveitis. METHODS In 14 patients with inactive Behçet's uveitis and 26 control individuals (13 with nonocular Behçet's syndrome and 13 healthy subjects), we analyzed the retinal nerve fiber layer, ganglion cell layer, full retinal thickness, foveal avascular zone area and sectorial parafoveal vascular density in the superficial vascular plexus, intermediate capillary plexus, and deep capillary plexus using SPECTRALIS optical coherence tomography (OCT) 2 and OCT angiography. Macular sensitivity was analyzed using an MP-3 microperimeter. RESULTS Eighteen eyes (78%) had a best-corrected visual acuity ≥ 20/25. Significant differences were found in Behçet's uveitis in comparison with the controls on the OCT and OCT angiography: 14.8%, 22.4%, and 14.9% ganglion cell layer thinning in the global, nasal, and inferior sectors, respectively; 6%, 13.2%, and 7.5% full retinal thickness thinning in the superior, nasal, and inferior sectors; and 16.8%, 14.9%, 23.6%, 15.8%, and 12.6% mean deep capillary plexus density reduction in the global, superior, nasal, inferior, and temporal sectors. Microperimetry data demonstrated significant mean reductions of 21% and 23.6% in central and average macular sensitivities and 28.8%, 40.4%, 27.7%, and 24.2% in the superior, nasal, inferior, and temporal sectors, respectively. Outer plexiform layer elevations were observed in Behçet's uveitis (69.6%). CONCLUSION Behçet's uveitis presented structural and functional macular damage despite good best-corrected visual acuity, mainly affecting the nasal sector and the deep capillary plexus. On OCT and OCT angiography, quantitative and qualitative changes can be valuable biomarkers of ocular involvement in Behçet's syndrome.
Collapse
Affiliation(s)
- Bruno F A Ferreira
- Department of Ophthalmology, Hospital das Clinicas HCFMUSP, LIM 33, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil; and
| | - Alex H Higashi
- Department of Ophthalmology, Hospital das Clinicas HCFMUSP, LIM 33, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil; and
| | - Leandro L Prado
- Rheumatology Division, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil
| | - Célio R Gonçalves
- Rheumatology Division, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil
| | - Maria A O Haddad
- Department of Ophthalmology, Hospital das Clinicas HCFMUSP, LIM 33, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil; and
| | - Leandro C Zacharias
- Department of Ophthalmology, Hospital das Clinicas HCFMUSP, LIM 33, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil; and
| | - Carlos E Hirata
- Department of Ophthalmology, Hospital das Clinicas HCFMUSP, LIM 33, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil; and
| | - Joyce H Yamamoto
- Department of Ophthalmology, Hospital das Clinicas HCFMUSP, LIM 33, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil; and
| |
Collapse
|
|
2
|
Jin J, Vinay K, Miller RE. Monitoring retinal pathology and cerebral injury in sickle cell disease using spectral-domain optical coherence tomography in pediatric patients. Pediatr Blood Cancer 2021; 68:e29028. [PMID: 33788385 PMCID: PMC8638774 DOI: 10.1002/pbc.29028] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/10/2020] [Revised: 03/08/2021] [Accepted: 03/09/2021] [Indexed: 11/09/2022]
Abstract
PURPOSE This study aimed to confirm the correlation between sickle cell disease (SCD) genotype and retinal damage identified by spectral-domain optical coherence tomography (SD-OCT), and examine a potential link between hypoxic ischemic injury in the retina and brain. METHODS In this prospective, observational case series, 117 patients (56 males) aged 5-20 years with SCD (36 SC, 68 SS, eight Sβ+ thalassemia, five Sβ0 thalassemia) underwent ophthalmologic examination including funduscopy and SD-OCT imaging. Comparison of SCD genotypes and association between ocular findings and cerebrovascular disease (CVD) in subjects with SS/Sβ0 genotype were investigated. RESULTS Visual acuity ranged from 20/20 to 20/40. On funduscopic exam, 16 of 117 (13.7%) had retinopathy; 69 of 117 (59.0%) showed inner retina thinning on SD-OCT. Patients with SS/Sβ0 showed a higher frequency of sickle cell retinopathy (SCR) change (68.5% vs. 47.2%), bilateral SCR (49.9% vs. 25.0%), and foveal involvement (15.1% vs. 0) than the SC genotype. While funduscopic findings in our cohort with SS/Sβ0 genotype showed no correlation with CVD, 20 of 21 patients with CVD had abnormal SD-OCT. Elevated reticulocyte percentage and aspartate aminotransferase are associated with SD-OCT changes and CVD. CONCLUSIONS SD-OCT was better than funduscopy in detecting retinal changes, higher frequency, and more extensive retinal changes in the more severe SCD genotypes SS and Sβ0 as compared with SC. The correlation between abnormal SD-OCT and CVD strongly suggests that retinal exam using SD-OCT may aid in detection and monitoring SCD-related CVD. Retinopathy may be another component of the hemolytic subphenotype of SCD.
Collapse
Affiliation(s)
- Jing Jin
- Division of Pediatric Ophthalmology, Nemours/Alfred l. duPont Hospital for Children, Wilmington, DE
| | - Kandula Vinay
- Department of Radiology, Nemours/Alfred l. duPont Hospital for Children, Wilmington, DE
| | - Robin E. Miller
- Center for Cancer and Blood Disorders, Nemours/Alfred l. duPont Hospital for Children, Wilmington, DE
| |
Collapse
|
|
3
|
Past, present and future role of retinal imaging in neurodegenerative disease. Prog Retin Eye Res 2021; 83:100938. [PMID: 33460813 PMCID: PMC8280255 DOI: 10.1016/j.preteyeres.2020.100938] [Citation(s) in RCA: 67] [Impact Index Per Article: 16.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2020] [Revised: 12/11/2020] [Accepted: 12/17/2020] [Indexed: 02/08/2023]
Abstract
Retinal imaging technology is rapidly advancing and can provide ever-increasing amounts of information about the structure, function and molecular composition of retinal tissue in humans in vivo. Most importantly, this information can be obtained rapidly, non-invasively and in many cases using Food and Drug Administration-approved devices that are commercially available. Technologies such as optical coherence tomography have dramatically changed our understanding of retinal disease and in many cases have significantly improved their clinical management. Since the retina is an extension of the brain and shares a common embryological origin with the central nervous system, there has also been intense interest in leveraging the expanding armamentarium of retinal imaging technology to understand, diagnose and monitor neurological diseases. This is particularly appealing because of the high spatial resolution, relatively low-cost and wide availability of retinal imaging modalities such as fundus photography or OCT compared to brain imaging modalities such as magnetic resonance imaging or positron emission tomography. The purpose of this article is to review and synthesize current research about retinal imaging in neurodegenerative disease by providing examples from the literature and elaborating on limitations, challenges and future directions. We begin by providing a general background of the most relevant retinal imaging modalities to ensure that the reader has a foundation on which to understand the clinical studies that are subsequently discussed. We then review the application and results of retinal imaging methodologies to several prevalent neurodegenerative diseases where extensive work has been done including sporadic late onset Alzheimer's Disease, Parkinson's Disease and Huntington's Disease. We also discuss Autosomal Dominant Alzheimer's Disease and cerebrovascular small vessel disease, where the application of retinal imaging holds promise but data is currently scarce. Although cerebrovascular disease is not generally considered a neurodegenerative process, it is both a confounder and contributor to neurodegenerative disease processes that requires more attention. Finally, we discuss ongoing efforts to overcome the limitations in the field and unmet clinical and scientific needs.
Collapse
|
|
4
|
Fickweiler W, Wolfson EA, Paniagua SM, Yu MG, Adam A, Bahnam V, Sampani K, Wu IH, Musen G, Aiello LP, Shah H, Sun JK, King GL. Association of Cognitive Function and Retinal Neural and Vascular Structure in Type 1 Diabetes. J Clin Endocrinol Metab 2021; 106:1139-1149. [PMID: 33378459 PMCID: PMC7993575 DOI: 10.1210/clinem/dgaa921] [Citation(s) in RCA: 17] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2020] [Indexed: 12/13/2022]
Abstract
CONTEXT Cognitive dysfunction is a growing and understudied public health issue in the aging type 1 diabetic population and is difficult and time-consuming to diagnose. Studies in long duration type 1 diabetes have reported the presence of proliferative diabetic retinopathy was associated with cognitive dysfunction. OBJECTIVE This study assessed whether structural and vascular abnormalities of the retina, representing an extension of the central nervous system, are associated with cognitive impairment and other complications of type 1 diabetes. METHODS An observational cross-sectional study of individuals with 50 or more years of type 1 diabetes (Joslin Medalist Study) was conducted at a university hospital in the United States. The study included 129 participants with complete cognitive testing. Validated cognitive testing measures included psychomotor speed, and immediate, and delayed memory. Optical coherence tomography (OCT) and OCT angiography (OCTA) were performed to obtain neural retinal layer thicknesses and vascular density for superficial (SCP) and deep retinal capillary plexus (DCP). Multivariable modeling was adjusted for potential confounders associated with outcomes in unadjusted analyses. RESULTS Decreased vessel density of the SCP and DCP was associated with worse delayed memory (DCP: P = .002) and dominant hand psychomotor speed (SCP: P = .01). Thinning of the retinal outer nuclear layer was associated with worse psychomotor speed both in nondominant and dominant hands (P = .01 and P = .05, respectively). Outer plexiform layer thickness was associated with delayed memory (P = .04). CONCLUSION These findings suggest that noninvasive retinal imaging using OCT and OCTA may assist in estimating the risks for cognitive dysfunction in people with type 1 diabetes.
Collapse
Affiliation(s)
- Ward Fickweiler
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Beetham Eye Institute, Joslin Diabetes Center, Boston, Massachusetts, USA
| | - Emily A Wolfson
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
| | | | - Marc Gregory Yu
- Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
| | - Atif Adam
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
| | - Vanessa Bahnam
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
| | - Konstantina Sampani
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Beetham Eye Institute, Joslin Diabetes Center, Boston, Massachusetts, USA
| | - I-Hsien Wu
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
| | - Gail Musen
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
| | - Lloyd P Aiello
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Beetham Eye Institute, Joslin Diabetes Center, Boston, Massachusetts, USA
- Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA
| | - Hetal Shah
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
| | - Jennifer K Sun
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Beetham Eye Institute, Joslin Diabetes Center, Boston, Massachusetts, USA
- Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA
| | - George L King
- Research Division, Joslin Diabetes Center, Boston, Massachusetts, USA
- Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
- Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA
| |
Collapse
|
|
5
|
Jusufovic M, Elsais A, Kerty E. Seven Points That Explain the Lack of Effect from Reperfusion Therapy in Central Retinal Artery Occlusion. Ophthalmol Retina 2019; 3:713-715. [PMID: 31511166 DOI: 10.1016/j.oret.2019.05.014] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/08/2019] [Revised: 05/13/2019] [Accepted: 05/15/2019] [Indexed: 11/27/2022]
Affiliation(s)
- Mirza Jusufovic
- Department of Neurology, Oslo University Hospital Rikshospitalet, Oslo, Norway
| | - Ahmed Elsais
- Department of Neurology, Oslo University Hospital Rikshospitalet, Oslo, Norway
| | - Emilia Kerty
- Department of Neurology, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway
| |
Collapse
|
|
6
|
Türkcü FM, Şahin A, Karaalp Ü, Çınar Y, Şahin M, Özkurt ZG, Keklikçi U. Automated quantification of foveal avascular zone and vascular density in Behçet's disease. Ir J Med Sci 2019; 189:349-354. [PMID: 31267410 DOI: 10.1007/s11845-019-02051-2] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/08/2019] [Accepted: 06/20/2019] [Indexed: 11/26/2022]
Abstract
PURPOSE To measure the vascular density (VD) and foveal avascular zone (FAZ) area in patients with Behçet's disease (BD) obtained by optical coherence tomography angiography (OCTA). METHODS VD and FAZ area in the deep and superficial retinal vascular networks were measured in all eyes. RESULTS Thirty BD and 31 control subjects were included in the study. The mean overall VD measured in the entire scan was lower in BD compared with control group in both the superficial (49.52 ± 6.54 vs 53.57 ± 2.87%, respectively; p = 0.003) and deep (53.44 ± 7.44 vs 58.41 ± 3.01%, respectively; p = 0.002) areas. The FAZ in the BD group was significantly increased at the level of the superficial (0.52 ± 0.67 vs 0.28 ± 0.1 mm2, respectively; p = 0.05) and deep (0.91 ± 1.25 vs 0.39 ± 0.14 mm2, respectively; p = 0.024) areas compared with those of the control group. The deep and the superficial FAZ areas were positively correlated with disease duration and negatively with VA. CONCLUSION In the patients with BD, OCTA showed decreased VD in both the superficial and deep retinal vascular networks. Besides, the VA was correlated with the VD and FAZ.
Collapse
Affiliation(s)
| | - Alparslan Şahin
- Department of Ophthalmology, Batman Zilan Hospital, Batman, Turkey
| | - Ümit Karaalp
- Department of Ophthalmology, Batman State Hospital, Batman, Turkey
| | - Yasin Çınar
- School of Medicine, Department of Ophthalmology, Dicle University, Diyarbakir, Turkey
| | - Muhammed Şahin
- School of Medicine, Department of Ophthalmology, Dicle University, Diyarbakir, Turkey.
| | - Zeynep Gürsel Özkurt
- School of Medicine, Department of Ophthalmology, Dicle University, Diyarbakir, Turkey
| | - Uğur Keklikçi
- School of Medicine, Department of Ophthalmology, Dicle University, Diyarbakir, Turkey
| |
Collapse
|
|
7
|
Van Keer K, Van Keer J, Barbosa Breda J, Nassiri V, De Deyne C, Genbrugge C, Abegão Pinto L, Stalmans I, Vandewalle E. Non-invasive assessment of cerebral oxygenation: A comparison of retinal and transcranial oximetry. PLoS One 2018; 13:e0190612. [PMID: 29304150 PMCID: PMC5755852 DOI: 10.1371/journal.pone.0190612] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/10/2017] [Accepted: 12/18/2017] [Indexed: 12/02/2022] Open
Abstract
BACKGROUND To investigate the correlation between cerebral (SO2-transcranial), retinal arterial (SaO2-retinal) and venous (SvO2-retinal) oxygen saturation as measured by near-infrared spectroscopy (NIRS) and retinal oximetry respectively. METHODS Paired retinal and cerebral oxygen saturation measurements were performed in healthy volunteers. Arterial and venous retinal oxygen saturation and diameter were measured using a non-invasive spectrophotometric retinal oximeter. Cerebral oxygen saturation was measured using near-infrared spectroscopy. Correlations between SO2-transcranial and retinal oxygen saturation and diameter measurements were assessed using Pearson correlation coefficients. Lin's concordance correlation coefficient (CCC) and Bland-Altman analysis were performed to evaluate the agreement between SO2-transcranial as measured by NIRS and as estimated using a fixed arterial:venous ratio as 0.3 x SaO2-retinal + 0.7 x SvO2-retinal. The individual relative weight of SaO2-retinal and SvO2-retinal to obtain the measured SO2-transcranial was calculated for all subjects. RESULTS Twenty-one healthy individuals aged 26.4 ± 2.2 years were analyzed. SO2-transcranial was positively correlated with both SaO2-retinal and SvO2-retinal (r = 0.44, p = 0.045 and r = 0.43, p = 0.049 respectively) and negatively correlated with retinal venous diameter (r = -0.51, p = 0.017). Estimated SO2-transcranial based on retinal oximetry showed a tolerance interval of (-13.70 to 14.72) and CCC of 0.46 (95% confidence interval: 0.05 to 0.73) with measured SO2-transcranial. The average relative weights of SaO2-retinal and SvO2-retinal to obtain SO2-transcranial were 0.31 ± 0.11 and 0.69 ± 0.11, respectively. CONCLUSION This is the first study to show the correlation between retinal and cerebral oxygen saturation, measured by NIRS and retinal oximetry. The average relative weight of arterial and venous retinal oxygen saturation to obtain the measured transcranial oxygen saturation as measured by NIRS, approximates the established arterial:venous ratio of 30:70 closely, but shows substantial inter-individual variation. These findings provide a proof of concept for the role of retinal oximetry in evaluating cerebral oxygenation.
Collapse
Affiliation(s)
- Karel Van Keer
- Department of Ophthalmology, University Hospitals Leuven, Leuven, Belgium
| | - Jan Van Keer
- Department of Cardiology, University Hospitals Leuven, Leuven, Belgium
| | - João Barbosa Breda
- Department of Ophthalmology, University Hospitals Leuven, Leuven, Belgium
| | | | - Cathy De Deyne
- Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium
- Department of Anesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium
| | - Cornelia Genbrugge
- Faculty of Medicine and Life Sciences, Hasselt University, Hasselt, Belgium
- Department of Anesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium
| | - Luís Abegão Pinto
- Department of Ophthalmology, Centro Hospitalar Lisboa Norte, Lisbon, Portugal
| | - Ingeborg Stalmans
- Department of Ophthalmology, University Hospitals Leuven, Leuven, Belgium
- Department of Ophthalmology Neurosciences, Laboratory of Ophthalmology, KU Leuven, Leuven, Belgium
| | - Evelien Vandewalle
- Department of Ophthalmology, University Hospitals Leuven, Leuven, Belgium
| |
Collapse
|
|
8
|
Nguyen CTO, Hui F, Charng J, Velaedan S, van Koeverden AK, Lim JKH, He Z, Wong VHY, Vingrys AJ, Bui BV, Ivarsson M. Retinal biomarkers provide "insight" into cortical pharmacology and disease. Pharmacol Ther 2017; 175:151-177. [PMID: 28174096 DOI: 10.1016/j.pharmthera.2017.02.009] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]
Abstract
The retina is an easily accessible out-pouching of the central nervous system (CNS) and thus lends itself to being a biomarker of the brain. More specifically, the presence of neuronal, vascular and blood-neural barrier parallels in the eye and brain coupled with fast and inexpensive methods to quantify retinal changes make ocular biomarkers an attractive option. This includes its utility as a biomarker for a number of cerebrovascular diseases as well as a drug pharmacology and safety biomarker for the CNS. It is a rapidly emerging field, with some areas well established, such as stroke risk and multiple sclerosis, whereas others are still in development (Alzheimer's, Parkinson's, psychological disease and cortical diabetic dysfunction). The current applications and future potential of retinal biomarkers, including potential ways to improve their sensitivity and specificity are discussed. This review summarises the existing literature and provides a perspective on the strength of current retinal biomarkers and their future potential.
Collapse
Affiliation(s)
- Christine T O Nguyen
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia.
| | - Flora Hui
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Jason Charng
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Shajan Velaedan
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Anna K van Koeverden
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Jeremiah K H Lim
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Zheng He
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Vickie H Y Wong
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Algis J Vingrys
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Bang V Bui
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| | - Magnus Ivarsson
- Department of Optometry and Vision Sciences, University of Melbourne, Parkville, 3010, Victoria, Australia
| |
Collapse
|
|
9
|
Cabrera DeBuc D, Somfai GM, Koller A. Retinal microvascular network alterations: potential biomarkers of cerebrovascular and neural diseases. Am J Physiol Heart Circ Physiol 2016; 312:H201-H212. [PMID: 27923786 DOI: 10.1152/ajpheart.00201.2016] [Citation(s) in RCA: 83] [Impact Index Per Article: 9.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/01/2016] [Revised: 11/04/2016] [Accepted: 11/11/2016] [Indexed: 12/12/2022]
Abstract
Increasing evidence suggests that the conditions of retinal microvessels are indicators to a variety of cerebrovascular, neurodegenerative, psychiatric, and developmental diseases. Thus noninvasive visualization of the human retinal microcirculation offers an exceptional opportunity for the investigation of not only the retinal but also cerebral microvasculature. In this review, we show how the conditions of the retinal microvessels could be used to assess the conditions of brain microvessels because the microvascular network of the retina and brain share, in many aspects, standard features in development, morphology, function, and pathophysiology. Recent techniques and imaging modalities, such as optical coherence tomography (OCT), allow more precise visualization of various layers of the retina and its microcirculation, providing a "microscope" to brain microvessels. We also review the potential role of retinal microvessels in the risk identification of cerebrovascular and neurodegenerative diseases. The association between vision problems and cerebrovascular and neurodegenerative diseases, as well as the possible role of retinal microvascular imaging biomarkers in cerebrovascular and neurodegenerative screening, their potentials, and limitations, are also discussed.
Collapse
Affiliation(s)
- Delia Cabrera DeBuc
- Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, Florida;
| | - Gabor Mark Somfai
- Semmelweis University, Budapest, Hungary.,Augenzentrum, Pallas Kliniken, Olten, Switzerland
| | - Akos Koller
- Institute of Natural Sciences, University of Physical Education, Budapest, Hungary; and.,Department of Physiology, New York Medical College, Valhalla, New York
| |
Collapse
|
|
10
|
Durham JT, Dulmovits BM, Cronk SM, Sheets AR, Herman IM. Pericyte chemomechanics and the angiogenic switch: insights into the pathogenesis of proliferative diabetic retinopathy? Invest Ophthalmol Vis Sci 2015; 56:3441-59. [PMID: 26030100 DOI: 10.1167/iovs.14-13945] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
Abstract
PURPOSE To establish the regulatory roles that pericytes have in coordinating retinal endothelial cell (EC) growth and angiogenic potential. METHODS Pericytes were derived from donor diabetic (DHuRP) or normal (NHuRP) human retinae, and characterized using vascular markers, coculture, contraction, morphogenesis, and proliferation assays. To investigate capillary "cross-talk," pericyte-endothelial coculture growth, and connexin-43 (Cx43) expression assays were performed. Paracrine effects were examined via treating EC with pericyte-derived conditioned media (CM) in proliferation, angiogenesis, and angiocrine assays. The effects of sphingosine 1-phosphate (S1P) were assessed using receptor antagonists. RESULTS The DHuRP exhibit unique proliferative and morphologic properties, reflecting distinctive cytoskeletal and isoactin expression patterns. Unlike NHuRP, DHuRP are unable to sustain EC growth arrest in coculture and display reduced Cx43 expression. Further, CM from DHuRP (DPCM) markedly stimulates EC proliferation and tube formation. Treatment with S1P receptor antagonists mitigates DPCM growth-promotion in EC and S1P-mediated pericyte contraction. Angiocrine assays on normal and diabetic pericyte secretomes reveal factors involved in angiogenic control, inflammation, and metabolism. CONCLUSIONS Effects from the diabetic microenvironment appear sustainable in cell culture: pericytes derived from diabetic donor eyes seemingly possess a "metabolic memory" in vitro, which may be linked to original donor health status. Diabetes- and pericyte-dependent effects on EC growth and angiogenesis may reflect alterations in bioactive lipid, angiocrine, and chemomechanical signaling. Altogether, our results suggest that diabetes alters pericyte contractile phenotype and cytoskeletal signaling, which ultimately may serve as a key, initiating event required for retinal endothelial reproliferation, angiogenic activation, and the pathological neovascularization accompanying proliferative diabetic retinopathy.
Collapse
|
|
11
|
Nakaizumi A, Fukumoto M, Kida T, Suzuki H, Morishita S, Satou T, Oku H, Ikeda T, Nakamura K. Measurement of serum and vitreous concentrations of anti-type II collagen antibody in diabetic retinopathy. Clin Ophthalmol 2015; 9:543-7. [PMID: 25848204 PMCID: PMC4376299 DOI: 10.2147/opth.s75422] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022] Open
Abstract
Background Autoimmune mechanisms have been postulated as a cause of diabetic retinopathy (DR), as several autoantibodies have reportedly been detected in the serum of DR patients. In this present study, we measured serum and vitreous levels of anti-type II collagen (anti-II-C) antibodies in DR patients and investigated their association with the mechanism of development of DR. Patients and methods Blood samples were obtained from patients with proliferative DR and from patients with diabetic macular edema who underwent vitrectomy at Osaka Medical College, Takatsuki City, Osaka, Japan. Diabetic patients without DR were also included. The control group consisted of age- and sex-matched patients with noninflammatory eye diseases who underwent eye surgery for retinal detachment or for cataracts. The levels of anti-II-C immunoglobulin (Ig)G antibody in the vitreous and serum were measured using a human/monkey anti-II-C IgG assay kit. Results The serum levels of anti-II-C IgG antibody were significantly higher in the DR patients than in the patients with noninflammatory eye disease (56.8±33.8 units/mL versus 30.5±13.7 units/mL, respectively; P<0.05, Fisher’s exact test). These levels were also significantly higher in the diabetic patients without DR than in the patients with noninflammatory eye disease (76.3±49.7 units/mL versus 30.5±13.7 units/mL, respectively; P<0.01, Fisher’s exact test). However, anti-II-C IgG antibody levels were unable to be detected in all of the obtained vitreous fluid samples. Conclusion The development and progression of DR may be related to a mechanism involving intraocular type II collagen, which normally has immunological tolerance as a sequestered antigen. In DR, the disruption of the blood–retinal barrier leads to contact between the intraocular type II collagen and immunocompetent cells, and to subsequent activation of the autoimmune mechanism.
Collapse
Affiliation(s)
- Atsuko Nakaizumi
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Masanori Fukumoto
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Teruyo Kida
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Hiroyuki Suzuki
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Seita Morishita
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Takaki Satou
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Hidehiro Oku
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | - Tsunehiko Ikeda
- Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, Japan
| | | |
Collapse
|
|
12
|
Satirtav G, Oltulu R, Kerimoglu H. Current evidence of pathophysiology of diabetic macular edema: A review. World J Ophthalmol 2014; 4:147-151. [DOI: 10.5318/wjo.v4.i4.147] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/17/2014] [Revised: 08/26/2014] [Accepted: 09/17/2014] [Indexed: 02/06/2023] Open
Abstract
Diabetic macular edema (DME) is an important cause of vision loss in patients with diabetes mellitus. The pathophysiology of DME can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the events that cause the edema to become chronic. On a macrocellular level, DME is believed to be in part caused by alterations in hydrostatic and oncotic pressures and shear stress. Angiogenic factor expression, inflammation and oxidative stress constitute the key components of microvascular pathways. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. Macular edema is thought to be caused as a result of these consequences.
Collapse
|
|
13
|
MacCormick IJC, Beare NAV, Taylor TE, Barrera V, White VA, Hiscott P, Molyneux ME, Dhillon B, Harding SP. Cerebral malaria in children: using the retina to study the brain. ACTA ACUST UNITED AC 2014; 137:2119-42. [PMID: 24578549 PMCID: PMC4107732 DOI: 10.1093/brain/awu001] [Citation(s) in RCA: 80] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
Cerebral malaria is a dangerous complication of Plasmodium falciparum infection, which takes a devastating toll on children in sub-Saharan Africa. Although autopsy studies have improved understanding of cerebral malaria pathology in fatal cases, information about in vivo neurovascular pathogenesis is scarce because brain tissue is inaccessible in life. Surrogate markers may provide insight into pathogenesis and thereby facilitate clinical studies with the ultimate aim of improving the treatment and prognosis of cerebral malaria. The retina is an attractive source of potential surrogate markers for paediatric cerebral malaria because, in this condition, the retina seems to sustain microvascular damage similar to that of the brain. In paediatric cerebral malaria a combination of retinal signs correlates, in fatal cases, with the severity of brain pathology, and has diagnostic and prognostic significance. Unlike the brain, the retina is accessible to high-resolution, non-invasive imaging. We aimed to determine the extent to which paediatric malarial retinopathy reflects cerebrovascular damage by reviewing the literature to compare retinal and cerebral manifestations of retinopathy-positive paediatric cerebral malaria. We then compared retina and brain in terms of anatomical and physiological features that could help to account for similarities and differences in vascular pathology. These comparisons address the question of whether it is biologically plausible to draw conclusions about unseen cerebral vascular pathogenesis from the visible retinal vasculature in retinopathy-positive paediatric cerebral malaria. Our work addresses an important cause of death and neurodisability in sub-Saharan Africa. We critically appraise evidence for associations between retina and brain neurovasculature in health and disease, and in the process we develop new hypotheses about why these vascular beds are susceptible to sequestration of parasitized erythrocytes.
Collapse
Affiliation(s)
- Ian J C MacCormick
- 1 Malawi-Liverpool-Wellcome Trust Clinical Research Programme, PO Box 30096, Chichiri, Blantyre 3, Malawi2 University of Liverpool, Department of Eye and Vision Science, Faculty of Health & Life Sciences, University of Liverpool Room 356, 4th Floor, UCD Building, Daulby Street, Liverpool L69 3GA, UK
| | - Nicholas A V Beare
- 2 University of Liverpool, Department of Eye and Vision Science, Faculty of Health & Life Sciences, University of Liverpool Room 356, 4th Floor, UCD Building, Daulby Street, Liverpool L69 3GA, UK3 Royal Liverpool University Hospital, St. Paul's Eye Unit, Prescot St, Liverpool, Merseyside L7 8XP, UK
| | - Terrie E Taylor
- 5 Blantyre Malaria Project, Blantyre, Malawi6 Michigan State University, Department of Osteopathic Medical Specialities, West Fee Hall, 909 Fee Road, Room B305, East Lansing, MI 48824, USA
| | - Valentina Barrera
- 2 University of Liverpool, Department of Eye and Vision Science, Faculty of Health & Life Sciences, University of Liverpool Room 356, 4th Floor, UCD Building, Daulby Street, Liverpool L69 3GA, UK
| | - Valerie A White
- 7 Vancouver General Hospital, Department of Pathology and Laboratory Medicine, Vancouver, B.C. V5Z1M9, Canada
| | - Paul Hiscott
- 2 University of Liverpool, Department of Eye and Vision Science, Faculty of Health & Life Sciences, University of Liverpool Room 356, 4th Floor, UCD Building, Daulby Street, Liverpool L69 3GA, UK
| | - Malcolm E Molyneux
- 1 Malawi-Liverpool-Wellcome Trust Clinical Research Programme, PO Box 30096, Chichiri, Blantyre 3, Malawi4 University of Malawi College of Medicine, College of Medicine, P/Bag 360 Chichiri, Blantyre 3 Malawi8 Liverpool School of Tropical Medicine, Liverpool School of Tropical Medicine, Pembroke Place , Liverpool, L3 5QA , UK
| | - Baljean Dhillon
- 9 University of Edinburgh, Department of Ophthalmology, Edinburgh, UK10 Princess Alexandra Eye Pavilion, Edinburgh, UK
| | - Simon P Harding
- 2 University of Liverpool, Department of Eye and Vision Science, Faculty of Health & Life Sciences, University of Liverpool Room 356, 4th Floor, UCD Building, Daulby Street, Liverpool L69 3GA, UK3 Royal Liverpool University Hospital, St. Paul's Eye Unit, Prescot St, Liverpool, Merseyside L7 8XP, UK
| |
Collapse
|
|
14
|
Pathogenic role of diabetes-induced PPAR-α down-regulation in microvascular dysfunction. Proc Natl Acad Sci U S A 2013; 110:15401-6. [PMID: 24003152 DOI: 10.1073/pnas.1307211110] [Citation(s) in RCA: 112] [Impact Index Per Article: 9.3] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
Two independent clinical studies have reported that fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist, has robust therapeutic effects on microvascular complications of diabetes, including diabetic retinopathy (DR) in type 2 diabetic patients. However, the expression and function of PPARα in the retina are unclear. Here, we demonstrated that PPARα is expressed in multiple cell types in the retina. In both type 1 and type 2 diabetes models, expression of PPARα, but not PPARβ/δ or PPARγ, was significantly down-regulated in the retina. Furthermore, high-glucose medium was sufficient to down-regulate PPARα expression in cultured retinal cells. To further investigate the role of PPARα in DR, diabetes was induced in PPARα knockout (KO) mice and wild-type (WT) mice. Diabetic PPARα KO mice developed more severe DR, as shown by retinal vascular leakage, leukostasis, pericyte loss, capillary degeneration, and over-expression of inflammatory factors, compared with diabetic WT mice. In addition, overexpression of PPARα in the retina of diabetic rats significantly alleviated diabetes-induced retinal vascular leakage and retinal inflammation. Furthermore, PPARα overexpression inhibited endothelial cell migration and proliferation. These findings revealed that diabetes-induced down-regulation of PPARα plays an important role in DR. Up-regulation or activation of PPARα may represent a novel therapeutic strategy for DR.
Collapse
|
|
15
|
Berkowitz BA, Bissig D, Dutczak O, Corbett S, North R, Roberts R. MRI biomarkers for evaluation of treatment efficacy in preclinical diabetic retinopathy. ACTA ACUST UNITED AC 2013; 7:393-403. [PMID: 23786440 DOI: 10.1517/17530059.2013.814639] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
INTRODUCTION One sober consequence of the current epidemic of diabetes mellitus is that an increasing number of people world-wide will partially or completely lose their sight to diabetic retinopathy. Clinically, the sight-threatening complications of diabetes are diagnosed and treated based on visible retinal lesions (e.g., dot-blot hemorrhages or retinal neovascularization). However, such anatomical microvascular lesions are slow to respond with treatment. Thus, there remains an urgent need for imaging biomarkers that are abnormal before retinal lesions are visibly apparent and are responsive to treatment. AREAS COVERED Here, the development of new MRI methods, such as manganese-enhanced MRI, for evaluating early diabetes-evoked retinal pathophysiology, and its usefulness in guiding new treatments for diabetic retinopathy are reviewed. EXPERT OPINION In diabetic retinopathy, not all important diagnostic and prognostic needs are well served by optical methods. In the absence of gross anatomy changes, critical times when drug intervention is most likely to be successful at reducing vision loss are missed by most light-based methods and thus provide little help in guiding diagnosis and treatment. For example, before clinical symptoms, is there an optimal time to intervene with drug therapy? Is a drug reaching its target? How does one assess optimal drug dose, schedule, and routes? How well do current experimental models mimic the clinical condition? As discussed herein, MRI is as an analytical tool for addressing these unmet needs. Future clinical applications of MRI can be envisioned such as in clinical trials to assess drug treatment efficacy, or as an adjunct approach to refine or clarify a difficult clinical case. New MRI-generated hypotheses about the pathogenesis of diabetic retinopathy and its treatment are discussed. In the coming years, a substantial growth in the development and application of MRI is expected to address relevant question in both the basic sciences and in the clinic.
Collapse
Affiliation(s)
- Bruce A Berkowitz
- Wayne State University, Department of Anatomy and Cell Biology, Detroit, MI, USA.
| | | | | | | | | | | |
Collapse
|
|
16
|
Dietrich N, Hammes HP. Retinal digest preparation: a method to study diabetic retinopathy. METHODS IN MOLECULAR BIOLOGY (CLIFTON, N.J.) 2013; 933:291-302. [PMID: 22893415 DOI: 10.1007/978-1-62703-068-7_19] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
Abstract
Retinal digestion is a commonly used method for studying experimental diabetic retinopathy in animal models. The method allows to assess qualitatively and quantitatively the morphology of the retinal vasculature, including characteristics of endothelial cells and pericytes. The digestion method uses the enzyme trypsin and enables the precise evaluation of venolar and arteriolar diameters, endothelial cell and pericyte numbers, and the formation of acellular capillaries.
Collapse
Affiliation(s)
- Nadine Dietrich
- 5th Medical Department, Universitätsmedizin Mannheim, University of Heidelberg, Mannheim, Germany
| | | |
Collapse
|
|
17
|
Ueda K, Nakahara T, Hoshino M, Mori A, Sakamoto K, Ishii K. Retinal blood vessels are damaged in a rat model of NMDA-induced retinal degeneration. Neurosci Lett 2010; 485:55-9. [DOI: 10.1016/j.neulet.2010.08.061] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/30/2010] [Revised: 08/18/2010] [Accepted: 08/20/2010] [Indexed: 11/24/2022]
|
|
18
|
Aging increases retinal vascular lesions characteristic of early diabetic retinopathy. Biogerontology 2010; 11:447-55. [DOI: 10.1007/s10522-010-9263-x] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/07/2009] [Accepted: 01/15/2010] [Indexed: 01/12/2023]
|
|
19
|
Abstract
String vessels are thin connective tissue strands, remnants of capillaries, with no endothelial cells; they do not carry blood flow. They occur in numerous species, particularly in the central nervous system, but can occur in any tissue where capillaries have died. String vessels are often associated with pathologies such as Alzheimer's disease, ischemia, and irradiation, but are also found in normal human brains from preterm babies to the aged. They provide a record of the original blood vessel location, but gradually disappear after months or years. There have been numerous studies of string vessels (acellular capillaries) in the retina, because retinal vessels can be seen in great detail in whole mounts after trypsin digestion. Capillary regression occurs by apoptosis, synchronously along capillary segments, with macrophages engulfing apoptotic endothelial cells. Macrophages may cause the apoptosis, or the regression may be triggered by loss of the endothelial cell survival factor VEGF. VEGF expression is induced by hypoxia and promotes capillary growth. Cessation of blood flow eliminates the shear stress that helps maintain endothelial cell survival. Capillaries can re-grow by proliferation and migration of endothelial cells into empty basement membrane tubes, which provide a structural scaffold, replete with signaling molecules. This is a problem in tumor control, but useful for recovery from capillary loss. There is an age-related waning of VEGF expression in response to hypoxia. This causes an age-related decline in cerebral angiogenesis and results in neuronal loss. It may also contribute to the proposed age-related loss of brain reserve.
Collapse
Affiliation(s)
- William R Brown
- Department of Radiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
| |
Collapse
|
|
20
|
Pournaras CJ, Rungger-Brändle E, Riva CE, Hardarson SH, Stefansson E. Regulation of retinal blood flow in health and disease. Prog Retin Eye Res 2008; 27:284-330. [PMID: 18448380 DOI: 10.1016/j.preteyeres.2008.02.002] [Citation(s) in RCA: 410] [Impact Index Per Article: 24.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Optimal retinal neuronal cell function requires an appropriate, tightly regulated environment, provided by cellular barriers, which separate functional compartments, maintain their homeostasis, and control metabolic substrate transport. Correctly regulated hemodynamics and delivery of oxygen and metabolic substrates, as well as intact blood-retinal barriers are necessary requirements for the maintenance of retinal structure and function. Retinal blood flow is autoregulated by the interaction of myogenic and metabolic mechanisms through the release of vasoactive substances by the vascular endothelium and retinal tissue surrounding the arteriolar wall. Autoregulation is achieved by adaptation of the vascular tone of the resistance vessels (arterioles, capillaries) to changes in the perfusion pressure or metabolic needs of the tissue. This adaptation occurs through the interaction of multiple mechanisms affecting the arteriolar smooth muscle cells and capillary pericytes. Mechanical stretch and increases in arteriolar transmural pressure induce the endothelial cells to release contracting factors affecting the tone of arteriolar smooth muscle cells and pericytes. Close interaction between nitric oxide (NO), lactate, arachidonic acid metabolites, released by the neuronal and glial cells during neural activity and energy-generating reactions of the retina strive to optimize blood flow according to the metabolic needs of the tissue. NO, which plays a central role in neurovascular coupling, may exert its effect, by modulating glial cell function involved in such vasomotor responses. During the evolution of ischemic microangiopathies, impairment of structure and function of the retinal neural tissue and endothelium affect the interaction of these metabolic pathways, leading to a disturbed blood flow regulation. The resulting ischemia, tissue hypoxia and alterations in the blood barrier trigger the formation of macular edema and neovascularization. Hypoxia-related VEGF expression correlates with the formation of neovessels. The relief from hypoxia results in arteriolar constriction, decreases the hydrostatic pressure in the capillaries and venules, and relieves endothelial stretching. The reestablished oxygenation of the inner retina downregulates VEGF expression and thus inhibits neovascularization and macular edema. Correct control of the multiple pathways, such as retinal blood flow, tissue oxygenation and metabolic substrate support, aiming at restoring retinal cell metabolic interactions, may be effective in preventing damage occurring during the evolution of ischemic microangiopathies.
Collapse
Affiliation(s)
- Constantin J Pournaras
- Department of Ophthalmology, Vitreo-Retina Unit, University Hospitals of Geneva, 22 rue Alcide Jentzer, CH-1211 Geneva 14, Switzerland.
| | | | | | | | | |
Collapse
|
|
21
|
Patton N, Aslam T, Macgillivray T, Pattie A, Deary IJ, Dhillon B. Retinal vascular image analysis as a potential screening tool for cerebrovascular disease: a rationale based on homology between cerebral and retinal microvasculatures. J Anat 2005; 206:319-48. [PMID: 15817102 PMCID: PMC1571489 DOI: 10.1111/j.1469-7580.2005.00395.x] [Citation(s) in RCA: 549] [Impact Index Per Article: 27.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/20/2023] Open
Abstract
The retinal and cerebral microvasculatures share many morphological and physiological properties. Assessment of the cerebral microvasculature requires highly specialized and expensive techniques. The potential for using non-invasive clinical assessment of the retinal microvasculature as a marker of the state of the cerebrovasculature offers clear advantages, owing to the ease with which the retinal vasculature can be directly visualized in vivo and photographed due to its essential two-dimensional nature. The use of retinal digital image analysis is becoming increasingly common, and offers new techniques to analyse different aspects of retinal vascular topography, including retinal vascular widths, geometrical attributes at vessel bifurcations and vessel tracking. Being predominantly automated and objective, these techniques offer an exciting opportunity to study the potential to identify retinal microvascular abnormalities as markers of cerebrovascular pathology. In this review, we describe the anatomical and physiological homology between the retinal and cerebral microvasculatures. We review the evidence that retinal microvascular changes occur in cerebrovascular disease and review current retinal image analysis tools that may allow us to use different aspects of the retinal microvasculature as potential markers for the state of the cerebral microvasculature.
Collapse
Affiliation(s)
- Niall Patton
- Princess Alexandra Eye Pavilion, Chalmers Street, Edinburgh, UK.
| | | | | | | | | | | |
Collapse
|
|
22
|
Burns MS, Bellhorn RW, Korte GE, Heriot WJ. Chapter 10 Plasticity of the retinal vasculature. ACTA ACUST UNITED AC 1986. [DOI: 10.1016/0278-4327(86)90013-1] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
|