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Retinal parameters, cortical cerebral microinfarcts, and their interaction with cognitive impairment
Saima Hilalhttps://orcid.org/0000-0001-5434-56351,2,3, Carol Y Cheung4, Tien Yin Wong5,6, Leopold Schmetterer5,6, and Christopher Chen1,2
Background:
Quantitative changes in retinal vessels and thinning of optic nerves have been associated with subclinical (atherosclerosis, inflammation) and clinical age-related brain pathologies (stroke and neurodegeneration). However, data on the association between both retinal vascular and neuronal parameters with cortical cerebral microinfarcts (CMIs) and how these factors jointly influence cognition are lacking.
Aim:
We investigated the association of retinal vascular and neuronal changes with CMIs on 3 T MRI
and explored their interaction with cognitive impairment in a memory-clinic population.
Methods:
A total of 538 participants were included. Retinal vascular parameters (caliber, tortuosity, and fractal dimension) were measured from retinal fundus photographs using a semi-automated computer-assisted program. Retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GC-IPL) thicknesses were obtained from optical coherence tomography. Cortical CMIs were defined as hypointense on T1-weighted MRI, <5 mm in diameter and restricted to the cortex. Cognition was assessed using Clinical Dementia Rating Sum-of-Boxes (CDR-SoB) score and detailed neuropsychological test. Multivariable regression analysis was conducted adjusting for age, sex, hypertension, hyperlipidemia, diabetes mellitus, smoking, diagnosis, white matter hyperintensities volume, lacunes, and cerebral microbleeds.
Results:
Larger venular caliber (Rate ratios (RR): 1.15, 95% CI: 1.01–1.38, p = 0.014), increased venular fractal dimension (RR: 1.58, 95% CI: 1.31–1.91, p ⩽ 0.001), increased venular tortuosity (RR: 1.54, 95% CI: 1.35–1.75, p ⩽ 0.001), and thinner GC-IPL (RR: 1.24, 95% CI: 1.13–1.36, p ⩽ 0.001) were associated with CMI counts. Among individuals in highest tertile of retinal parameters, a significant interaction was observed between venular tortuosity (RR: 1.12, 95% CI: 1.02–1.22, p-interaction = 0.014) and GC-IPL (RR: 1.05, 95% CI: 1.01–1.11, p-interaction < 0.001) with CMIs on CDR-SoB.
Conclusion:Retinal vascular and neuronal parameters are associated with cortical CMIs, and persons with both pathologies are likely to have cognitive impairment. Further studies may be warranted to evaluate the clinical utility of retinal parameters and CMI in risk prediction for cognitive dysfunction.
Conclusion:Retinal vascular and neuronal parameters are associated with cortical CMIs, and persons with both pathologies are likely to have cognitive impairment. Further studies may be warranted to evaluate the clinical utility of retinal parameters and CMI in risk prediction for cognitive dysfunction.
Keywords
Cortical microinfarcts, cognition, retina
1Memory Aging and Cognition Center, National University Health System, Singapore, Singapore
2Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
3Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore, Singapore
4Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong, China
5Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore
6Ophthalmology and Visual Sciences Academic Clinical Program, Duke-NUS Medical School, Singapore, Singapore
Corresponding author(s):
Saima Hilal, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Level 4, Block MD3, 16 Medical Drive, Singapore 117600, Singapore. Email: phchs@nus.edu.sg
Introduction
In addition to the traditional MRI markers of vascular injury such as lacunar infarcts and white matter hyperintensities (WMH), a novel marker of cerebrovascular disease (CeVD), cortical cerebral microinfarcts (CMIs) have gained increasing attention because of its major role in cognitive impairment and dementia.1 This is in part due to CMIs recently being made visible in-vivo using conventional imaging techniques, hence enabling study of the impact of these lesions on brain structural and functional damage during life.2,3
The retina and optic nerve are outgrowths of the embryonic diencephalon and, therefore, share anatomic similarities, and functional and immunological characteristics with the brain.4,5 The presence of ocular manifestations in neurodegenerative and cerebrovascular pathologies, such as Alzheimer’s disease (AD) and stroke, emphasizes the strong relationship between the eye and the brain.6–8 Retinal changes in particular serve as a surrogate for cerebral changes in these disorders. Offering a “window to the brain,” the transparent eye enables non-invasive imaging of these changes in retinal structure and vasculature.
Previous studies have shown that quantitative changes in retinal vessel width (narrower arteriolar caliber and wider venules) have been associated with subclinical (lacunes and WMH) and clinical age-related brain diseases.9 Furthermore, smaller fractal dimensions reflecting a sparser branching pattern were associated with cerebral microbleeds and lacunar infarcts.10,11 Similarly, thinning of the optic nerve has been associated with cerebral infarcts.12,13 However, data on the association between both retinal vascular and neuronal parameters with cortical CMIs are lacking. Given the influence of retinal changes and cortical CMIs on brain vasculature and their common involvement in cognitive impairment and AD, the interaction of these two factors is of interest to better understand how they jointly give rise to cognitive impairment. So far, previous studies have only examined the individual effects of retinal changes and cortical CMIs on other imaging correlates and cognitive dysfunction without examining their possible interaction. We, therefore, investigated the association of retinal vascular and neuronal changes with cortical CMIs on 3 T MRI and explored their interaction in relation to cognitive impairment in a memory-clinic population. We first hypothesize that persons with altered retinal parameters (e.g., wider and more tortuous venules, thinner retinal neuronal layer) are likely to have higher counts of CMIs on MRI scans. Second, persons with both CMI and retinal changes are more likely to have cognitive impairment.
1Memory Aging and Cognition Center, National University Health System, Singapore, Singapore
2Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
3Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore, Singapore
4Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong, China
5Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore
6Ophthalmology and Visual Sciences Academic Clinical Program, Duke-NUS Medical School, Singapore, Singapore
Corresponding author(s):
Saima Hilal, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Level 4, Block MD3, 16 Medical Drive, Singapore 117600, Singapore. Email: phchs@nus.edu.sg
Introduction
In addition to the traditional MRI markers of vascular injury such as lacunar infarcts and white matter hyperintensities (WMH), a novel marker of cerebrovascular disease (CeVD), cortical cerebral microinfarcts (CMIs) have gained increasing attention because of its major role in cognitive impairment and dementia.1 This is in part due to CMIs recently being made visible in-vivo using conventional imaging techniques, hence enabling study of the impact of these lesions on brain structural and functional damage during life.2,3
The retina and optic nerve are outgrowths of the embryonic diencephalon and, therefore, share anatomic similarities, and functional and immunological characteristics with the brain.4,5 The presence of ocular manifestations in neurodegenerative and cerebrovascular pathologies, such as Alzheimer’s disease (AD) and stroke, emphasizes the strong relationship between the eye and the brain.6–8 Retinal changes in particular serve as a surrogate for cerebral changes in these disorders. Offering a “window to the brain,” the transparent eye enables non-invasive imaging of these changes in retinal structure and vasculature.
Previous studies have shown that quantitative changes in retinal vessel width (narrower arteriolar caliber and wider venules) have been associated with subclinical (lacunes and WMH) and clinical age-related brain diseases.9 Furthermore, smaller fractal dimensions reflecting a sparser branching pattern were associated with cerebral microbleeds and lacunar infarcts.10,11 Similarly, thinning of the optic nerve has been associated with cerebral infarcts.12,13 However, data on the association between both retinal vascular and neuronal parameters with cortical CMIs are lacking. Given the influence of retinal changes and cortical CMIs on brain vasculature and their common involvement in cognitive impairment and AD, the interaction of these two factors is of interest to better understand how they jointly give rise to cognitive impairment. So far, previous studies have only examined the individual effects of retinal changes and cortical CMIs on other imaging correlates and cognitive dysfunction without examining their possible interaction. We, therefore, investigated the association of retinal vascular and neuronal changes with cortical CMIs on 3 T MRI and explored their interaction in relation to cognitive impairment in a memory-clinic population. We first hypothesize that persons with altered retinal parameters (e.g., wider and more tortuous venules, thinner retinal neuronal layer) are likely to have higher counts of CMIs on MRI scans. Second, persons with both CMI and retinal changes are more likely to have cognitive impairment.
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